Optic nerve evaluation among optometrists.

PURPOSE: To determine agreement among optometrists regarding assessment of optic nerve C/D ratios and perceived glaucomatous damage and to separately analyze these results on the basis of residency training, practice setting, and glaucoma patient experience. METHODS: Fifty-six optometrists from various modes of professional practice evaluated 33 stereoscopic optic nerve photographs. Observers were asked to estimate the vertical cup-to-disk (C/D) ratio and determine the glaucomatous status of the optic nerve. The mean vertical C/D ratio, percentage perceived as glaucomatous, and levels of interobserver and intraobserver agreement (kappa) are reported. RESULTS: Estimated C/D ratios differ significantly on the basis of training (p = 0.02) practice setting (p = 0.001), glaucoma patient experience (p = 0.001). Glaucomatous damage interpretation was significantly different (p = 0.006) based upon an optometrist's practice setting. Interobserver agreement regarding C/D ratios is significantly higher among optometrists who have completed a residency (kappaw = 0.59) and practice in clinical settings (optometry school/medical center/hospital) (kappaw = 0.59) compared with non-residency-trained optometrists (kappaw = 0.52) and those practicing in commercial settings (kappaw = 0.54). Interobserver agreement of glaucomatous damage is significantly higher among optometrists who have completed a residency (kappa = 0.50) compared with non-residency-trained optometrists (kappa = 0.42). CONCLUSIONS: Intraobserver agreement is higher than interobserver agreement among optometrists when C/D ratios are estimated and the glaucomatous status of the optic nerve is assessed. Optic nerve evaluation among optometrists is significantly influenced by residency training, practice setting, and glaucoma patient encounters.

Central serous chorioretinopathy and HIV.

BACKGROUND: Patients with central serous chorioretinopathy (CSC) have sudden-onset, painless, uniocular blur that is typically diagnosed via fundus and fluorescein angiographic appearance. The etiology and pathophysiology are not fully understood; however, there may be an association with an infectious etiology. This article presents two cases of HIV-positive patients in whom central serous chorioretinopathy developed and discusses the possible relationship between the two cases. The differential diagnosis, clinical features, angiographic appearance, management options, and proposed etiologies of CSC will be presented. CASE REPORTS: A 34-year-old black man HIV reported to the eye clinic with decreased vision in his right eye. A diagnosis of central serous chorioretinopathy (CSC) was made on the basis of the clinical and fluorescein appearance. He is currently being monitored for resolution. A 44-year-old black man with profoundly compromised immunity also came to the eye clinic with CSC and HIV retinopathy. He later progressed to CMV retinitis and subsequently died. CONCLUSION: Although considered in many cases to be idiopathic, central serous chorioretinopathy has been associated with infectious etiologies, one of which could be HIV.

Congophilic angiopathy of the brain: a clinical and pathological report on two siblings.

Clinical and histological accounts are given of a sister and brother, dying aged 61 and 56 years respectively after illnesses lasting 5-6 years marked by a progressive mental and physical disability. The family history suggested transmission by a dominant gene. The histological findings were of a very severe congophilic angiopathy confined to the brain, spinal cord and leptomeninges and giving rise to multiple haemorrhages and softenings. There were, in addition, abundant amyloid-containing "plaques" of various forms, found principally in the hippocampus and cerebellar cortex. The cases are compared with similar cases in the literature, and reasons given for regarding this condition as a separate entity rather than a variant of Alzheimer's disease.

Cardiovascular control in recently injured tetraplegics in spinal shock.

Cardiovascular control was studied in five tetraplegic patients with physiologically complete cervical spinal cord transections. All had been injured less than two weeks previously and were in spinal shock. Blood pressure, heart rate, and plasma noradrenaline and adrenaline were measured at rest and during and after bladder stimulation and application of cold stimuli to skin below the level of the lesion. In three patients the cardiovascular responses to intravenously infused 1-noradrenaline and to the Valsalva manoeuvre were recorded. Measurements were also made in six chronic tetraplegic patients (in whom reflex spinal cord activity had returned) at rest, and during and after bladder stimulation, and in six normal subjects at rest. Average resting blood pressure in the recently injured tetraplegics was 130/57 (mean 81) mmHg, in the chronic tetraplegics 107/55 (mean 73) mmHg and in normal subjects 122/82 (mean 95) mmHg. Average resting heart rate was 64, 73 and 77 beats/min in the three groups respectively. Resting plasma noradrenaline and adrenaline levels in both the recently injured and chronic tetraplegics were lower than than in normal subjects. In the recently injured tetraplegics bladder stimulation caused minimal changes in blood pressure, heart rate and plasma noradrenaline and adrenaline levels. In the chronic tetraplegics similar stimulation caused marked hypertension, bradycardia and elevation in plasma noradrenaline but not adrenaline levels. Cold stimuli in the recently injured tetraplegics did not change blood pressure or heart rate. In the recently injured tetraplegics intravenous infusion of 1-noradrenaline resulted in greater elevation in blood pressure than normal. There was a decrease in heart rate. One patient was able to perform the Valsalva manoeuvre. His blood pressure responses were consistenly abnormal ('blocked' Valsalva).

Postural changes in plasma renin activity and responses to vasoactive drugs in a case of Shy-Drager syndrome.

A male aged 47 years with gross autonomic insufficiency as part of the Shy-Drager syndrome is described. He did not sweat normally when warmed, and his circulatory responses to mental arithmetic, the Valsalva manoeuvre, and head-up tilt were abnormal indicating severe sympathetic failure. During head-up tilt there was a rise in plasma renin activity and plasma aldosterone. It is argued that plasma renin activity is not dependent on sympathetic nervous activity and may be mediated by renal baroreceptors. These rises may help sustain the blood pressure in such patients during repeated head-up tilts. Infusions of L-noradrenaline and angiotension produced greater hypertension, and injections of isoprenaline greater hypotension than in controls. Although it is difficult to exclude the possibility that one factor in this may be hypersensitivity of receptors in blood vessel walls, the principal factor is likely to be the absence of those baroreflexes of which the efferent pathways are in the sympathetic nervous system.

Enhanced pressor response to noradrenaline in patients with cervical spinal cord transection.

Arterial blood pressure, heart-rate and the electrocardiogram were recorded in subjects tetraplegic from cervical spinal cord transections, and in control subjects, before, during and after intravenous infusions of 1-noradrenaline. Over a wide range of doses the blood pressure rose much more in the tetraplegics than in the controls. Circulating noradrenaline during infusion did not significantly differ between the two groups. The findings indicate that tetraplegic subjects have an enhanced pressor response to noradrenaline infusions. Such a response therefore does not necessarily indicate post-ganglionic sympathetic denervation. The observed responses in the tetraplegics may in part be due to exaggerated adrenergic receptor responses, but the main cause is likely to be the loss of those baroreceptor reflexes with sympathetic efferent pathways.

Plasma catecholamines during paroxysmal neurogenic hypertension in quadriplegic man.

Blood pressure, heart rate, and plasma catecholamine levels were measured in 16 quadriplegic subjects with physiologically complete cervical spinal cord transections above the level of the sympathetic outflow, and in 15 normal subjects (controls). In the quadriplegics the average resting blood pressure was 107/59 (mean, 75) mmHg, heart rate was 65 beats/min, and plasma norepinephrine (NE) and epinephrine (E) levels were 0.05 and 0.005 ng/ml, respectively. In the controls average resting blood pressure was 117/79 (mean, 92) mmHg, heart rate was 61 beats/min, and resting plasma NE and E levels were 0.20 and 0.06 ng/ml, respectively. Resting blood pressure and plasma NE and E levels were significantly lower in the quadriplegics (P less than 0.01, less than 0.001, less than 0.001, and less than 0.001, less than 0.001, respectively) than in the controls. In the quadriplegics, neurogenic hypertension was induced by bladder and muscle stimulation. This resulted in a marked elevation of both systolic and diastolic blood pressure (from an average of 109/60 (mean, 75) to 168/87 (mean, 114) mmHg) as a result of uninhibited sympathetic nervous activity through the isolated spinal cord. Plasma NE consistently rose, from an average of 0.05 to 0.16 ng/ml (P less than 0.001). There was significant linear relationship between plasma NE and mean blood pressure (P less than 0.001). In the quadriplegics infusion of l-norepinephrine to raise the blood pressure to comparable levels (from 105/58 (mean, 74) to 183/93 (mean, 123) mmHg) resulted in plasma NE levels approximately 21 times higher than during muscle and bladder stimulation. It is possible that the lower resting arterial blood pressure and plasma NE and E levels in the quadriplegics in comparison to normal subjects may reflect diminished resting sympathetic nervous activity. The rise in blood pressure following increased sympathetic nervous activity was accompanied by an elevation in plasma NE. The hypertension was not secondary to the rise in plasma NE. Plasma NE in these subjects appears to be a reliable index of prevailing sympathetic nervous activity.

Dopamine beta-hydroxylase release during hypertension from sympathetic nervous overactivity in man.

In subjects with cervical spinal cord transections, hypertension due to sympathetic nervous overactivity resulted in a rise in plasma dopamine beta-hydroxylase (DbetaH), the peak occurring 3 to 5 min after the peak blood pressure response. This indicates that DbetaH may be released from sympathetic nerve terminals during sympathetic activity in man, and emphasizes the importance of sample timing in acute studies on DbetaH.

Mechanisms of reflex cardiac arrest in tetraplegic patients.

Four patients with physiologically complete high cervical spinal-cord lesions, sustained within the previous 6 weeks, were observed. All needed intermittent positive-pressure ventilation. In the stage of spinal shock, stimuli to the trachea induced bradycardia, and in two patients cardiac arrest resulted. The bradycardia occurred when the patients were hypoxic, and seemed to be due to a vaso-vagal reflex. Normally this reflex is opposed by sympathetic activity, and during hypoxia by increased pulmonary (inflation) vagal reflex activity due to increased breathing. In these patients, however, compensatory sympathetic activity was prevented by the cervical cord lesion, and increased pulmonary vagal reflex activity by the fact that the breathing was artificial and therefore did not increase with hypoxia. Treatment in emergency includes the administration of atropine. Adequate oxygenation and, if this cannot be achieved, maintenance atropin should prevent the bradycardia and cardiac arrest associated with stimulation of the trachea in artificially ventilated tetraplegic patients.

Plasma prostaglandin E during neurogenic hypertension in tetraplegic man.

1. Arterial blood pressure and heart rate were measured before, during and after cutaneous and visceral stimulation in subjects tetraplegic due to severe cervical spinal cord damage. Stimulation resulted in marked hypertension as a result of reflex sympathetic overactivity. 2. Mixed venous blood from a catheter situated in the right atrium was obtained before and after stimulation and plasma prostaglandin E and prostaglandin F were measured. A consistent and significant rise in plasma prostaglandin E, but not plasma prostaglandin F, accompanied the hypertension. 3. It is suggested that prostaglan ding E is released during this sympathetic nervous activity and may be related to neurogenic hypertension.

Postoperative management after thymectomy.

This paper reports a retrospective study of the preoperative and postoperative management of 28 patients who underwent thymectomy between 1956 and 1973. Patients who received postoperative artificial ventilation were compared with the group who did not with respect to sex, age, severity of disease, preoperative vital capacity, and thymic histology. Evidence is presented that postoperative artificial ventilation is required when the preoperative vital capacity with the patient on optimum anticholinesterase treatment is less than 2 litres. Additional features associated with a probable need for artificial ventilation were the presence of a thymoma, bulbar symptoms, especially dysphagia, and age over 50 years. These should be taken into account in any patient whose vital capacity is close to the critical level of 2 litres. When postoperative ventilation was required it was usually necessary for 12 days or more, and tracheostomy should therefore be done at or before thymectomy. Most patients in this series received the same dose of anticholinesterases after operation as before it and no evidence was found of a sudden decrease in requirements for anticholinesterase therapy. Two patients did not, and in them a myasthenic crisis was precipitated. We propose that the preoperative drug regimen can be continued in the immediate postthymectomy period, allowing selection of patients for tracheostomy and artificial ventilation primarily on the basis of the preoperative vital capacity.

Late residua of acute idiopathic polyneuritis.

An account is given of four patients with acute idiopathic polyneuritis, leading within a few days to almost total paralysis. Two of these (cases 3 and 4) began to recover voluntary movement in the limbs in a month or less, and showed complete clinical recovery in three and 10 months respectively. The other two (cases 1 and 2) began to recover proximal limb movements after three months, reached a plateau of recovery in about two years, and never recovered movements in the distal parts of the limbs, which underwent muscular atrophy. Patient 2 died 14 years after the acute illness and was examined post mortem. The difference in recovery is explained by supposing that in patients 3 and 4 the lesions consisted predominantly of segmental demyelination, whereas in patients 1 and 2 there was extensive axon destruction at a proximal level. Recovery in the latter depended upon nerve regeneration, which restored the power of the proximal muscles, but was too slow for effective reinnervation of distal muscles. This explanation is supported by post mortem findings in patient 2. A further observation in patient 2 was of degeneration of the posterior white columns of the spinal cord, which was not due to loss of posterior root fibres. It is believed that in such cases a prognosis as to ultimate recovery of muscle power can be made about a month after the acute phase, according to whether movement has begun to return in the distal parts of the limbs. If recovery does not occur within two years it will not occur at all.

Hypotension in tetanus.

Three patients with severe tetanus had episodes of profound arterial hypotension lasting from minutes to hours. The blood pressure was recorded continuously for 13, 19, and six days respectively by an intra-arterial catheter, and other measurements included heart rate, central venous pressure, cardiac output, and blood gases.The hypotension was distinguished from that of "shock", for there was no clinical evidence of peripheral vasoconstriction and no tachycardia. It could not be attributed to disturbances of salt and water balance. During episodes of hypotension the blood pressure fell as low as 32/16 mm Hg, the heart rate fell from a mild tachycardia to normal values or a mild bradycardia, and the central venous pressure did not rise. The onset and the end of such episodes was often abrupt and the hypotension was often produced in response to a stimulus. In one patient extreme hypotension followed the aspiration of secretions from the trachea. These changes may represent another effect of tetanus on autonomic nervous activity, including impairment of baroreceptor reflexes.

Neurogenic muscle atrophy in myasthenia gravis.

Two cases of severe myasthenia gravis are described, with histological findings. Both cases showed severe neurogenic atrophy of the muscles of the tongue, with fatty pseudohypertrophy and a remarkable proliferation of terminal nerve fibres. Similar, but less severe, changes were present in other bulbar muscles. The findings are in keeping with the view that functional interruption at the neuromuscular junctions results first in failure to transmit the contractile impulse, and at a later stage in denervation atrophy. Terminal proliferation of axons is regarded as an attempt, on the part of motor fibres, to compensate for the breakdown of normal neuromuscular interaction.