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In 9 patients with congenital and acquired lesions of the optic radiation, videopupillographic investigations have been employed to determine the pupillographic threshold in the homonymous field defect. The study includes 3 patients suffering from congenital porencephalic cysts. The pupillary response was graded as akinetic, hypokinetic or eukinetic. These classifications yield some diagnostic clues as to the nature of the lesion. An attempt was made using the VER response in these patients to correlate the findings.

A pupillographic technique, an adaptation of the swinging light test, is described for the measurement of unilateral afferent pupillary defects. In normal persons it yielded accurate, reproducible estimates of the magnitude of artificial afferent defects made with neutral filters of 1 to 4 log units density. In 15 studies on 8 patients with unilateral optic neuritis and 2 with unilateral compressive lesions the measured afferent pupillary defects correlated closely with both visual acuity and visual threshold deficits. Measurement of the pupillary defect underestimated severe degrees of impairment revealed by visual threshold determination. Discrepancies between pupillary defect and visual acuity were observed in the 2 patients with compressive lesions and in 1 patient who had a central scotoma 4 months after an attack of optic neuritis.

Twenty-nine patients with presumed compressive optic neuropathy were studied, and pupil cycle times were measured. We found (1) normalcy of the test in cases of space-occupying lesion without suprasellar extension or after successful operation; (2) prolongation of pupil cycle time in cases of subclinical disorder conformed by visual evoked responses as well; (3) a good correlation between the values of prolonged pupil cycle time and degree of involvement of the visual field in pathological cases.

The clinical picture of metabolic encephalopathies has no aetiological specificity. It combines disturbances in conscious level dominated by disorientation and time and space and disturbances in motor activity, in particular tremor and asterixis. For each of the aetiologies studied, the following are considered: the circumstances of onset, the clinical and laboratory picture, the physiopathology and the treatment. From a diagnostic standpoint, particular emphasis should be placed upon the circumstances of onset which alone give any indication. The majority of these encephalopathies are caused by a lack of respect for simple rules in parenteral alimentation or by deficiencies. It is thus essentially an iatrogenic pathology. Treatment should be above all preventive.

Fifty-six patients with cysticercosis and neuro-ophthalmic signs were examined by me during an 11-year period. Their symptoms generally reflected increased intracranial pressure caused by hydrocephalus, subacute meningitis, cerebral masses or a combination of these effects. Papilledema (37 patients) was the commonest sign, with pupillary abnormalities (16 patients) and nystagmus (12 patients) frequently encountered. Cysticercosis is a relatively benign, although episodic, disease, as long as secondary obstructive hydrocephalus is promptly diagnosed and treated by CSF shunting procedures.

There is substantial evidence that prostaglandins (PG's) mediate acute elevations of intraocular pressure (IOP) due to laser irradiation of the iris. In the present study, we determined the optimal laser parameters needed to produce the maximal rise in IOP in anesthetized rabbits. Application of argon laser (0.75 watts, 0.5 sec. duration, and 8 spots of 500 micron size) to the iris of pigmented rabbits elicited an acute rise in IOP and miosis accompanied by an increase in aqueous protein concentration. This response was followed by a delayed ocular hypotension that lasted for more than 3 days and returned to baseline by day 5. The onset of ocular hypertension occurred within 15 min. and remained elevated for at least 90 min. The laser induced rise in IOP was related more to the number of laser spots applied to the iris than to the intensity of the total laser energy utilized. Pretreatment with either indomethacin or flurbiprofen produced a dose dependent inhibition of ocular hypertensive response and significantly reduced aqueous protein concentration. Indomethacin (0.01-30 mg/kg) was administered intraperitonially 1 hr. before laser treatment and flurbiprofen (0.03-0.3%) was administered topically 45 and 15 min. prior to laser application. The hypertensive response was reduced by more than 90% of control after both drugs, whereas the delayed hypotension was significantly antagonized only at the highest dose of indomethacin. Neither indomethacin nor flurbiprofen altered the maximum miotic response to laser irradiation of the iris. However, 0.3% flurbiprofen and 30 mg/kg indomethacin significantly increased the recovery rate of the miotic pupil. The results of this study support the contention that argon laser induced ocular hypertension may provide a quantitative assessment of inhibition of prostaglandin mediated responses.

Sequential cerebrospinal fluid (CSF) pressure-volume studies were carried out in seven cats during the expansion at a constant rate of an epidural balloon. The same studies were performed in three control cats. Beginning after 20 minutes of inflation and continuing to the point of pupillary dilatation there was a progressive increase in the pressure-volume index (volume required to change intracranial pressure (ICP) by tenfold). During the course of balloon inflation, there was also a progressive increase in CSF elastance (instantaneous ICP change per unit change in CSE volume). At the point of pupillary dilatation there was a marked, abrupt increase in the pressure-volume index and an equally dramatic decrease in CSF elastance. The CSF outflow resistance increased to a variable extent during balloon inflation. The plot of the CSF pressure versus balloon volume (the mass lesion pressure-volume curve) was of the classical configuration with an initial relatively flat segment and a final steep segment. A hypothesis is presented that interprets the shape of the mass lesion pressure-volume curve in terms of changes occurring in the elastic properties of the tissues surrounding the CSF space and the volume of the CSF space. It is proposed that this hypothesis will explain most of the commonly observed variations in CSF pressure. Confusion regarding the ICP-volume relationships has arisen because of lack of specificity regarding which anatomical spaces are being perturbed.

In recent years, the role of auditory evoked responses (AERs) in the intensive care unit (ICU) setting has expanded dramatically for both pediatric and adult brain-injured patient populations. AERs have unique value in early identification and evaluation of peripheral auditory dysfunction that can result directly from head trauma or as a consequence of intensive medical therapy (such as prolonged intubation and ototoxic drugs). AERs can also be applied in evaluating and monitoring neurologic status during the acute period following a severe brain injury, similar to their common intraoperative use as a neurophysiologic monitor. This paper reviews factors influencing measurement of AERs in the ICU, including the effect of (1) intensive medical therapy (e.g., neuromuscular blockers, sedatives, barbiturates, aminoglycosides, and loop diuretics); (2) coma; and (3) computed tomography confirmed temporal bone fracture. The rationale for monitoring neurologic status with AERs in this setting is presented and supported with original group data. Important points are illustrated with selected case reports.

Pupil cycle time was found to correlate with the clinical findings in 24 patients with noncompressive optic nerve pathology, including 11 cases of multiple sclerosis. Furthermore, subclinical multiple sclerosis was detected by the prolongation of pupil cycle time and was confirmed by visual evoked potential analysis. There was a correspondence between dynamics in the clinical findings and the pupil cycle time in two cases of multiple sclerosis that were followed up.

After covered fistulizing operations for primary glaucoma without complications the anterior chamber is deeper than it was prior to surgery. This means that the contact between the posterior surface of the iris and the lens may be very important in the pathogenesis of all primiary glaucomas, especially in acute primary glaucoma: an acute iridolenticular block can develop. Severe blocking mechanisms of the posterior surface of the iris sometimes appear after fistulizing glaucoma operations and after cataract extractions (with and without implantation of a pseudophakos) if there is no postoperative dilatation of th pupil. Peripheral iridectomies alone cannot prevent the anterior chamber from becoming shallower or flattened, possibly with the development of malignant glaucoma.

Ten cluster headache patients and 10 healthy controls were subjected to electrocardiographic and pupillometric procedures in a search for cardiac and pupillary sympathergic asymmetry. Sympathergic stimulation was provoked by hyperventilation and by instilling tyramine into both eyes. In the control group, hyperventilation changed neither the T-wave form and polarity nor the QTc. Tyramine provoked an equal mydriasis on the two sides. In cluster headache sufferers, hyperventilation produced changes in the T-wave form and polarity as well as an increase of the QTc due to a disproportionate shortening of the R-R and Q-T intervals. An unequal mydriasis was noted after tyramine instillation due to less marked response on the symptomatic side. The observed electrocardiographic abnormalities are considered an expression of an asynchronous repolarization attributed to a sympathergic asymmetry. It is postulated that both the cardiac and pupillary sympathetic imbalance associated with cluster headache are central in origin.

A simple portable pupillometer using Polaroid photography has been developed for use in the diagnosis of diabetic autonomic neuropathy. The pupil diameter per cent (PD%), defined as the percentage of iris diameter to which pupil diameter had dilated in darkness, was measured from the instant colour prints. An age-related normal range was constructed from measurements in 163 healthy subjects in whom PD% declined linearly by 3% per decade. The PD% was measured in 15 patients with automatic neuropathy and 12 were identified with abnormally low values indicating a failure of sympathetically mediated dilatation. Results were consistent with the standard television pupillometric technique and had the same high repeatability with a coefficient of variation of 3.2%.

Twenty-nine patients with cluster headache have been examined with the pupillometer and the evaporimeter. Pupils were dilated by sympathicomimetic drugs instilled into the conjunctival sacs, and responses of the two sides were compared. Forehead sweating was stimulated by body heating and by pilocarpine injection, and sweat evaporation on the two sides was compared. Most patients demonstrated the known patterns of hyposecretion on heating, of pilocarpine supersensitivity, and of deficient pupillary dilatation on OH-amphetamine stimulation on the symptomatic side and a supersensitivity of this pupil to phenylephrine. There were deviations from the rule for all methods of testing. Sixteen patients demonstrated a typical supersensitivity response of the pupil and of the sweat glands on the symptomatic side. Six patients had no such response, and seven patients had a discrepancy between the pupillary and the sweat gland response to stimulation, supersensitivity being present in one system only. There was a high degree of concordance between the results of the various methods of examination.

Accommodative disfacility and intermittent exotropia are two common clinically-observed ocular abnormalities. However, records of individual system dynamics are rare and mechanisms for possible interactive effects between the accommodation and the vergence system remain obscure in cases of system dysfunction. We present objective, quantitative, static and dynamic records of accommodation, vergence and related system responses in a symptomatic patient having accommodation disfacility and intermittent exotropia and propose that these two conditions worked in a pathogenic symbiotic manner.

Many primary care physicians perform only a superficial pupillary evaluation as part of the physical examination. The authors review several maneuvers that require no special equipment and help to improve diagnostic yield. The "swinging flashlight" test aids in detecting a relative afferent pupillary defect. When a patient has anisocoria, the initial diagnostic challenge is to determine which pupil is abnormal. Comparing the extent of pupillary inequality under both dim and bright illumination almost always identifies the dysfunctioning pupil(s) and narrows the differential diagnosis. The authors compare third-nerve palsy and Horner's syndrome as causes of anisocoria and review light-near dissociation, another important category of pupillary dysfunction. This latter phenomenon is seen in the Argyll Robertson pupil, the dorsal midbrain syndrome, and the tonic pupil syndromes. Pupillary size and activity are key diagnostic parameters in the evaluation of patients in coma. Structural and mechanical iris defects are also frequently responsible for pupillary anomalies.

The visual acuity of 100 patients between the ages of 16 and 66 years, seen for routine ophthalmologic examination, was measured before and after dilation. All patients had a predilation visual acuity of 20/40 or better. Postdilation binocular visual acuity using the patients' usual correction was measured first in the office and then outdoors, both with the patient's back to and the patient facing the sun, with and without the aid of postmydriatic sunglasses. Twelve percent experienced disabling photophobia even with the use of postmydriatic sunglasses, with 3% having significant objective visual loss defined as 20/50 or worse. No objective visual loss was found in 30 controls examined outdoors before dilation, without sunglasses. We recommend that patients who have experienced significant photophobia with dilation in the past, or who have never before undergone dilation, make arrangements for transportation after a dilated examination.

A 33-year-old white man developed premature presbyopia and anisocoria as initial manifestations of acute pandysautonomia. Nine months later signs and symptoms of generalized, severe autonomic dysfunction developed, and six years later only paralysis of pupillary reactions, presbyopia, and orthostatic hypotension were unresolved. Pharmacologic testing of the pupils demonstrated no mydriasis to cocaine 4% or hydroxyamphetamine 1% and hypersensitivity to epinephrine 0.1%, methacholine 2.5%, and pilocarpine 0.0625%, suggesting the presence of sympathetic and parasympathetic, postganglionic blockage of autonomic innervation of the iris.

Rapid reversal of fixed pupils, complete external 3rd nerve ophthalmoplegia, and coma occurred after early ventriculostomy in two hypertensive male patients with spontaneous intraventricular hemorrhage and secondary acute hydrocephalus. Putative pathophysiology of fixed pupils secondary to transtentorial herniation from obstructive hydrocephalus is discussed. Cases such as the present ones are unsettling because they are exceptions to the usually reliable negative prognosis indicated by fixed pupils. Nonetheless, it is important to report these cases to delineate which patients with this important clinical sign may benefit from aggressive management.

Pattern-reversal visual evoked potentials (VEP) were recorded in 41 patients suffering from syphilis in different stages. --In a latent syphilis 3 from 50 eyes (6%) had abnormal VEPs although ophthalmological findings were normal. --In neuro-syphilis, however, 16 from 32 eyes (50%) showed delayed responses. Ophthalmological findings were much less abnormal: visual acuity in 12%, visual field in 19%, and either or both of them in 25%. Pupillary disturbances were observed in 62%.

While primary neurologic damage in the patient with head trauma may be irreversible, damage from secondary injuries can often be avoided with rapid identification and correction of factors potentially leading to such injury. In patients with severe injuries, systematic evaluation is needed, including assessment of respiratory and circulatory systems, history taking, inspection of the head, and neurologic, general, and roentgenographic examination, as well as monitoring of vital functions, continuing patient care, and administration of intravenous fluids and medications.

In this study the variations in pupil diameter induced by different stimuli (dark-light adaptation, light reflex, electric stimulation of the sural nerve) were investigated in episodic (in the active or remission phases) and in chronic cluster headache (CH) patients. Pupil size monitoring was performed with a monocular, infrared TV pupillometer, and sural nerve stimuli were applied after the pain threshold had been measured as the flexion reflex threshold of the biceps femoris muscle (RIII reflex). The results were compared with those obtained in patients with "peripheral" (third neuron) Horner's syndrome and in healthy sex- and age-matched controls. On the symptomatic side we found an impairment of pupil response to light flashes and nociceptive stimuli; similar findings were sometimes evident on the pain-free side, too. These results substantiate previous observations that in cluster headache a dysfunction of the integrative central nervous system pathways also exists intercritically and mostly bilaterally, involving both autonomic regulation and pain perception mechanisms.

The significance of the dilated pupil in head injury is discussed. History of this condition and its possible mechanisms are described. Three patient reports are presented with unilateral dilated pupil. The literature on the subject is reviewed. Finally, the diagnostic steps which may be taken to differentiate direct third nerve injury from expanding mass lesion are suggested.

Besides of infrared-reflexphotometry several videosystems are used for pupillography. The main modification of our TV-pupillography consists of the connection of the infrared-camera with a videorecorder. Thus changes of the shape of the pupil can be evaluated continuously. Therefore, indications for our variant of pupillography are especially those types of anisocoria with loss of the round shape of the pupils.

Patients with congenital achromatopsia and congenital stationary night blindness have been known to show a transient pupillary constriction to darkness. We examined 50 normal subjects and 108 patients with retinal and optic nerve dysfunction to see if any had an initial pupillary constriction to darkness. We used a new infrared television apparatus. Four patients with congenital stationary night blindness, four with achromatopsia, two with bilateral optic neuritis, and one with dominant optic atrophy showed the phenomenon. In the patients who showed this unusual pupillary response to darkness it was the first observable event every time the lights were turned off. The constriction could usually be seen with a handlight, and it was similar in latency to the normal pupillary dilatation to darkness. Pupillary constriction to darkness is a clinically valuable sign that can be used in the detection of congenital retinal disease in children with poor vision.

Satisfactory visual results are reported in a series of 80 consecutive patients who underwent intracapsular cataract extraction with a four- or three-loop Binkhorst lens replacement. Nearly 50% of patients could see 20/30 or better unaided. However, results in the under 70 age group tend to be marred by macular edema, and in the over 80 age group by corneal edema, the latter occasionally being the result of lens instability because of an atonic pupil.

Three relatively clear-cut diagnostic groups, namely primary major depressive disorder-endogenous subtype (PRI MDD-E), primary anxiety disorder with no depression (PRI ANX), and normal controls as well as two additional patient groups with mixed or coexisting anxious/depressive diagnoses were studied. Clinical assessment was made by routine psychiatric interview, Schedule of Affective Disorder and Schizophrenia (SADS) research interview, and obtaining family history of MDD. Subjects underwent both routine 'baseline' sleep EEG polygraphic arecoline, a muscarinic, cholinergic agonist infused during sleep. Cholinergic sensitivity was assessed by measuring the time to induction of REM sleep after arecoline infusion. In addition, a subgroup of MDD patients underwent pupillographic testing. Peripheral alpha-adrenergic responsivity was measured by the magnitude of pupillary mydriatic response after local ocular instillation of phenylephrine. Successful separation (83% correct classification) of the 'pure' groups (PRI MDD-E, PRI ANX, and normal) was achieved by discriminant function analysis of sleep EEG variables. Compared to PRI ANX and normal groups, patients with PRI MDD-E had supersensitive cholinergic REM-induction response, shorter REM latency, increased first REM density and REM percent. Separation of the PRI ANX and normal groups was by intermittent awake time, delta sleep percent, and total REM density. Classification of the mixed anxious/depressive groups was next attempted using the discriminant coefficients derived from the above analysis of 'pure' groups. We found that the presence of absence of family history of MDD in patients with mixed diagnosis offered the best prediction of classification into PRI MDD-E and PRI ANX groups, respectively. MDD patients with coexisting panic disorder were significantly subsensitive to phenylephrine-induced mydriasis compared to MDD patients without anxiety.

The constriction-dilation cycles of pupils exposed to a stationary, discrete slit-lamp beam were significantly prolonged in 25 myasthenic patients (1,060.4 +/- 45.8 msec) undergoing therapy with steroids, anticholinesterases, or both, compared to normal controls (801.9 +/- 8.6 msec) or subjects receiving steroids for nonneurological disease (860.9 +/- 14.9 msec). The duration of myasthenia correlated with the slowing of the cycle time. Myasthenia gravis may affect ectodermally derived smooth muscle or the autonomic neuromuscular junction or both, and not be restricted to the well-demonstrated alterations of neuromuscular junction in striated muscle of mesodermal origin. Alternatively, prolonged pupillary cycles could be attributed to dysfunction of central pathways of the pupillary light reflex.

Intermittent corectopia was recently observed in a patient with bilateral, rostral midbrain infarction. Results from neuropathologic examination disclosed isolated but intact Edinger-Westphal nuclei. An explanation of midbrain corectopia centered on segmental innervation of the pupil by the Edinger-Westphal nucleus. In the presence of a paralyzed dilator muscle, select, central inhibition of sphincter tone resulted in an oval and eccentric pupil.

Studies on the nasal cycle have demonstrated that the autonomic tone to the nose is asymmetrical and oscillates in a regular cycle. Autonomic tone may be regulated from a centre in the hypothalamus and normally there is a balance between he autonomic tone of the right and left halves of the body. However, under stress or with hypothalamic instability this balance may be disrupted and result in the marked autonomic asymmetry seen in migraine or Meniér's syndrome. Research on the nasal cycle in conditions where autonomic asymmetry is apparent could change the entire concept of autonomic control.

Pupil changes provide vital information related to the cause and location, and at times, severity of disease processes which alter level of consciousness. Size and reactivity are sensitive to a variety of influences including local eye damage, functional state of brainstem, local systemic drugs, seizures and anoxia. Therefore, accurate measurement of pupillary size and reactivity is essential. The purposes of this study were to determine if pairs of nurses (1) achieved the same measurement of pupil sizes with and without an objective measure, and (2) selected the same descriptor for pupillary reaction to light. Sixty-eight pairs of nurses employed in adult and pediatric units of a large teaching hospital participated in the study. Interrater reliability of pupillary assessment of 136 nurses was determined. There was no significant difference in the reliability of nurses assessing pupillary size regardless of whether they used a penlight pupil gauge to measure or used observation without a pupil gauge. Agreement among the nurses on the pupillary size was high. Agreement on the pupillary reaction, however, was poor to good.

The effects are reported of acute and long-term continuous administration of three opiate antagonists--naloxone, naltrexone, and diprenorphine--on neurological function, survival, and infarct size in a feline model of acute focal cerebral ischemia. All three drugs produced statistically significant improvement in motor function following acute administration without concomitant changes in level of consciousness; saline had no effect. Naloxone and naltrexone significantly prolonged survival (p less than 0.01); diprenorphine did not. Infarct size was not altered by any treatment administered. These findings confirm previous work suggesting that, with the appropriate methodology, treatment with opiate antagonists partially reverses neurological deficits. They also show that opiate antagonists prolong survival in certain conditions of acute and subacute focal cerebral ischemia without altering the area of infarcted tissue.