Biomedical subjects

D E Cowen

Publications and source records attributed to D E Cowen.

18 recordsLinked to original sources

PubMed1999

Eyelid kinematics following blepharoplasty.

PURPOSE: This study characterizes the effects of blepharoplasty on blink dynamics in subjects with dermatochalasis. The authors evaluate the hypothesis that orbicularis oculi removal and the consequent alterations in blink are potentially harmful consequences of blepharoplasty. METHODS: Sixteen patients were studied, before and after laser blepharoplasty, by a modified scleral search coil technique. Changes in lid position during blinks were recorded before surgery as well as 2 months, and 1 year postoperatively. Off-line analyses assessed blink down-phase amplitude, peak velocity, duration, and main sequence (peak velocity versus amplitude) relationships. RESULTS: Despite muscle resection, there was no significant compromise of mean blink down-phase amplitude, peak velocity, or main sequence following blepharoplasty. Mean blink duration was likewise unchanged at either follow-up session from the preoperative state. Our data show that upper lid blepharoplasty does not cause any lasting decrement in lid function in blinking. CONCLUSIONS: Blepharoplasty includes resection of a portion of the orbicularis oculi. It appears unlikely that the purposeful resection of preseptal portion of the orbicularis oculi that accompanies blepharoplasty is responsible for any functional complications such as dry eye.

Adult↗

PubMed1998

Efficacy of gold weight implants in facial nerve palsy: quantitative alterations in blinking.

Deficient eyelid closure is a major visual threat to patients with unresolved facial nerve palsy. Gold weight implants assisted eyelid closure in patients with paresis of the orbicularis oculi, ameliorating patient complaints of dry eye, excessive tearing, and corneal epithelial breakdown. We used dynamic measures to assess the efficacy of upper eyelid gold weight implantation surgery for facial nerve palsy. The search coil technique was used to record spontaneous blinks bilaterally in six patients, before and after unilateral gold weight implantations into the upper eyelid in severe facial nerve palsy. In uncomplicated facial nerve palsy, the amplitude of blink down-phases for the paretic eyelid was 28.6 +/- 5.7% of the amplitude of the contralateral, normal eyelid. Following corrective surgery, closure of the paretic eyelid improved to 42.6 +/- 7.5% (P < 0.05). There was not a commensurate increase in the peak velocity of blink down-phases, suggesting that gold weight effects are mediated by a passive improvement in blink dynamics.

Adult↗

PubMed1997

The role of blink adaptation in the pathophysiology of benign essential blepharospasm.

OBJECTIVE: To investigate eyelid movements in patients with benign essential blepharospasm (BEB), with an emphasis on the characterization of the kinematics of normal and spastic blinks, assessment of interocular differences, and further delineation of the role of adaptive blink mechanisms in eyelid movement disorders. PATIENTS AND METHODS: The electromagnetic search coil technique was used to record the metrics of blinks bilaterally in 5 patients with untreated BEB. Eyelid kinematics and the main-sequence (peak velocity vs amplitude) relationships were analyzed. RESULTS: Patients with BEB exhibited a decrease in blink amplitude and peak velocity. Moreover, the main-sequence slope was decreased bilaterally. Spasms were bilateral and relatively conjugate. There was no change in the coordination of normal blinking across the 2 eyelids. CONCLUSIONS: These data demonstrate the operation of the adaptive regulation of blinking in an eyelid movement disorder. The findings suggest that the adaptive regulation of blink is a bilateral event. Blink-adaptive control systems can act on the blink reflex excitability and main-sequence relationships, changing these either together or independently. The hyperexcitable blink reflex of BEB is met by what is believed to be an adaptive decrease in the main-sequence slope that would decrease the strength of debilitating spasms. Collectively, these data extend the knowledge of the pathophysiology of BEB and, perhaps more important, establish the role of blink system plasticity in eyelid movement disorders.

Adaptation, Physiological↗

PubMed1997

Maladaptive neural compensatory mechanisms in Bell's palsy-induced blepharospasm.

We described four patients with Bell's palsy and blepharospasm and evaluated potential mechanisms that may be responsible for an apparent association between the two disorders. Eyelid movements in spontaneous blinks were studied by the search coil technique in patients with this novel disorder. Kinematic analyses documented bilateral eyelid spasm subsequent to unilateral Bell's palsy. The temporal interval between the onset of palsy and onset of blepharospasm was highly variable (weeks to > 20 years). Changes in the relationship between spontaneous blink peak velocity and amplitude, the main sequence, shared features previously found in uncomplicated Bell's palsy and blepharospasm patients. Furthermore, as in patients with typical Bell's palsy and idiopathic blepharospasm, both normal blinks and spasms were conjugate in spite of interocular differences in blink amplitude/peak velocity. We suggest that there is a correlation between the eyelid palsy and subsequent blepharospasm, and have designated this potentially new disease entity as Bell's palsy-induced blepharospasm. We propose a two-stage model for Bell's palsy-induced blepharospasm in which blink adaptive systems may produce the maladaptive consequence of eyelid spasms.

Adult↗

PubMed1996

Environmental tobacco smoke: a risk factor for pediatric laryngospasm.

Adult patients who smoke are known to have airway complications during general anesthesia. The objective of this study was to explore the relationship between environmental tobacco smoke (ETS) exposure in the home and laryngospasm during general anesthesia in pediatric patients. A retrospective, cohort study was performed on pediatric ambulatory patients in the day surgery center and main operating room of a university hospital. We studied 310 consecutive pediatric patients (all ASA physical status I) who underwent an outpatient elective ear, nose, and throat or urologic surgical procedure in the spring and summer of 1994, and received inhalation induction by mask with halothane. Laryngospasm was identified from quality management and anesthetic records, and included only those patients whose records indicated that succinylcholine was given because of oxygen desaturation and inability to ventilate. Patients' families were questioned within 1 wk after surgery as to the number of smokers in each child's household. Of 96 children with ETS exposure, 9 (9.4%) developed laryngospasm. Of the 214 patients without domestic ETS exposure, 2 (0.9%) developed laryngospasm. The relative risk for developing laryngospasm was 10 times higher in the ETS-exposed patients compared with the non-ETS-exposed group (95% confidence interval = 2.2-45.6; P < 0.001). We conclude that ETS exposure is a strong risk factor for laryngospasm in infants and children during general anesthesia.

Anesthesia, General↗

PubMed1995

The vascularized temporoparietal fascial flap for correction of the deep superior sulcus.

The deep superior sulcus is one of the more difficult problems to correct in the enophthalmic or anophthalmic orbit. Multiple procedures as well as materials have been proposed in recent years to address the cosmetic deformity. These methods have used a number of alloplastic and autogenous materials. Ideal correction of a soft tissue deformity uses well-vascularized autogenous tissue. This paper introduces the use of the temporoparietal fascial flap for correction of the deep superior sulcus. The advantages of this flap over other materials lies in its pliability, vascularity, thinness, ease of mobilization, and minimal subsequent donor site morbidity or deformity.

Adult↗

PubMed1993

Stenotic puncta: microsurgical punctoplasty.

The successful long-term management of epiphora caused by punctal stenosis presents a difficult problem for the ophthalmologist. The purpose of this paper is to describe a successful procedure that respects lacrimal excretory anatomy and provides excellent results in the management of epiphora. Twenty-three patients (32 eyes) with punctal stenosis underwent excision of the stenotic puncta followed by microscopic externalization of the vertical canaliculus. At 6 months and 1 year, only one patient complained of tearing; at 2 years, three eyes experienced tearing and were successfully dilated; no eyes experienced tearing at 4 years. Only one patient experienced a dry eye, which was managed with topical lubricants. Microscopic punctoplasty thus provides excellent long-term management of epiphora from punctal stenosis with minimal disruption of anatomy.

Aged↗

PubMed1988

Polyamine inhibition preserves somatosensory evoked potential activity after transient cerebral ischaemia.

We tested the hypothesis that the increase in polyamines observed after cerebral ischaemia is related to deficits in electrocortical function as measured by somatosensory evoked potential (SEP). Adult Mongolian gerbils were anaesthetized with ketamine and prepared for monitoring SEP, cerebral blood flow (CBF) in parietal and frontal regions by H2 clearance, and for bilateral carotid artery occlusion (BCO). Seven animals served as controls and received saline. Another 7 animals were treated with the ornithine decarboxylase inhibitor, difluoromethylornithine (DFMO) (100 mg/kg I.P.) just prior to 40 min BCO followed by 4 h reperfusion. With BCO, both CBF and SEP declined significantly. In control animals, CBF fell from basal 37.8 +/- 4.7 cc/100 g/min to 2.9 +/- 1.2 cc/100 g/min and recovered to 22.7 +/- 3.5 cc/100 g/h over the 4 h reperfusion period. DFMO treatment did not alter this CBF pattern. SEP amplitude declined to 11.3 +/- 3.2% basal during occlusion. DFMO preserved SEP during ischaemia (35.5 +/- 16.8% basal) and remained significantly more preserved during reperfusion (p less than 0.05). These results suggest that polyamines are involved in the progressive decline in neuroelectrical function which occurs during occlusion/reperfusion in the Mongolian gerbil. The observation that polyamine inhibition preserves electrical function despite not altering blood flow indicates that the effects of polyamines are not manifested at the level of the vasculature but perhaps at the neuronal membrane.

Animals↗

PubMed1988

Thromboxane synthetase inhibition with imidazole increases blood flow in ischemic penumbra.

Previous studies have indicated that the regional distribution of the arachidonic acid metabolites around a focal ischemic lesion may be important in the pathogenesis of cerebral ischemia. To determine the functional significance of this regionalization, we examined the effect of imidazole (a thromboxane synthetase inhibitor) on the distribution of the vasoconstrictor thromboxane and the vasodilators prostacyclin and prostaglandin E2 (PGE2) and on the distribution of cerebral blood flow (CBF) around a focal ischemic lesion, middle cerebral artery (MCA) occlusion in the cat. The study was conducted in two phases. The first phase examined regional distribution of tissue arachidonic acid metabolites and the effect of imidazole treatment on that distribution. The second phase examined the effect of imidazole treatment on the distribution of blood flow about the focal ischemic lesion as well as on electrocortical function and edema production. MCA occlusion resulted in increased thromboxane, prostacyclin, and PGE2 levels in the ipsilateral hemisphere. These increases were greatest in the region of marginal ischemia and were present both 3 and 6 hours after occlusion. Imidazole pretreatment (50 mg/kg i.p.) significantly inhibited thromboxane production, but augmented production of prostacyclin and PGE2. In the blood flow studies, imidazole was without effect on regions of dense cerebral ischemia (CBF less than 20 ml/minute/100 g for more than 12 of 24 postocclusion hours). In regions of marginal ischemia (20 less than CBF less than 30 ml/minute/100 g for more than 12 of 24 postocclusion hours), imidazole pretreatment significantly increased blood flow in both gray and white matter compared with saline-treated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1987

Measurement of somatosensory evoked potential in the Mongolian gerbil: the effects of cerebral ischaemia.

Normal somatosensory evoked potential (SEP) as well as changes after incomplete cerebral ischaemia following bilateral carotid artery occlusion (BCO) were characterized in the Mongolian gerbil. BCO significantly decreased cerebral blood flow (CBF). Reperfusion CBF at 10 min and 2, 3 and 4 h was significantly below preischaemic control values. BCO decreased SEP amplitude but had no effect on EP-P3 central conduction time. BCO did significantly increase EP-P11 central conduction time. Reperfusion amplitudes at 10 min and 2, 3 and 4 h revealed a significant increase only at 4 h when compared to the ischaemic amplitude. EP-P11 central conduction time at 10 min reperfusion showed dramatic improvement compared to ischaemic values, although values at 2, 3 and 4 h reperfusion were not statistically different from ischaemic values. A separate group of animals prepared identically but without BCO showed no significant changes in either SEP or CBF over time. These studies establish the protocol necessary to measure SEP in the Mongolian gerbil. In the future SEP may be used as an integral tool in the study of the primary determinants of neurophysiological recovery following cerebral ischaemia.

Animals↗

PubMed1987

Moderate hypothermia reduces postischemic edema development and leukotriene production.

Using the bilateral carotid artery occlusion model of cerebral ischemia in the gerbil, we studied the effect of moderate hypothermia (30 to 31 degrees C) on the postischemic production of prostanoids (cyclooxygenase pathway) and leukotrienes (lipoxygenase pathway) and accompanying changes in cerebral edema formation. Hypothermia capable of slowing central evoked potential conduction time was studied over the course of 40 minutes of cerebral ischemia and for up to 2 hours of reperfusion. The successful induction of cerebral ischemia was confirmed by somatosensory evoked potential amplitude changes. Measurements of 6-ketoprostaglandin F1 alpha (PGF1 alpha) and leukotriene B4 (LTB4) (radioimmunoassay) and cerebral edema (specific gravity) were made at early (10 minutes) and late (2 hours) reperfusion times. Although both white and gray matter showed no early significant difference in edema accumulation between normothermic and hypothermic gerbils at 10 minutes of reperfusion, hypothermic animals demonstrated significantly less white matter edema (specific gravity, 1.0397 +/- 0.0010 vs. 1.0341 +/- 0.0012, P less than 0.01) and gray matter edema (specific gravity, 1.0408 +/- 0.0009 vs. 1.0365 +/- 0.0008, P less than 0.01) by 2 hours of reperfusion. Production of PGF1 alpha was not significantly different between normothermic and hypothermic animals during the reperfusion period; however, hypothermic gerbils demonstrated significantly lower production of LTB4 at 10 minutes reperfusion time compared to normothermic animals (1.49 +/- 0.79 vs. 5.28 +/- 1.49 pg/mg of protein, P less than 0.05). This difference between the two groups in LTB4 levels was no longer detectable at 2 hours of reperfusion time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Lipoxygenase metabolites of arachidonic acid and the development of ischaemic cerebral oedema.

This study examined the changes in cerebral blood flow, water content, and lipoxygenase metabolites (leukotrienes) following bilateral carotid artery occlusion (BCO) and reperfusion in the gerbil. The effect of inhibiting lipoxygenase with nordihydroguaretic acid (NDGA) was also examined. BCO caused cerebral blood flow (measured using H2 clearance) to decline from 23.5 +/- 1.9 to 4.5 +/- 1.9 ml/min/100 gm. Reperfusion increased flow to 27.9 +/- 4 ml/min/100 gm at 10 min, which declined to 13.7 +/- 1.3 ml/min/100 gm at 50 min. Concomitant oedema measurement revealed brain specific gravity decreasing to 1.0402 +/- 0.0014 at 10 min and to 1.0325 +/- 0.0006 at 50 min reperfusion (nonoccluded controls). Leukotriene B4 (LTB4) increased from 26.8 +/- 4.6 to 33.5 +/- 2.1 pg/mg protein 10 min after reperfusion (p less than 0.05), but declined to 21.8 +/- pg/mg protein by 100 min (vs nonischaemic control = 21.3 +/- 2.9 pg/mg protein). Activation of arachidonate metabolism was confirmed by significantly increased 6 keto PGF1 alpha. Pretreatment of the animals with NDGA did not alter CBF, but increased specific gravity above saline-treated controls at 50 min of reperfusion (NDGA = 1.0370 +/- 0.002 vs control = 1.0325 +/- 0.0006, p less than 0.05). Similarly, NDGA blunted the increase in LTB4 formation 10 min after reperfusion (control = 26.8 +/- 4.6 pg/mg protein vs NDGA = 29.7 +/- 2.9 pg/mg protein, p = N.S.). These findings indicate that LTB4 production is stimulated by BCO and reperfusion in the gerbil, and that this stimulation occurs early on in the reperfusion. Further, we observe that the lipoxygenase inhibitor NDGA limits the formation of ischaemic cerebral oedema.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1986

Development of cyclooxygenase and lipoxygenase metabolites of arachidonic acid after transient cerebral ischemia.

Vasoactive arachidonic acid metabolites are postulated to play a role in the pathogenesis of cerebral ischemia. In order to characterize the local generation of cyclooxygenase and lipoxygenase metabolites of arachidonic acid in transient ischemia with reperfusion, Mongolian gerbils were studied for regional cerebral blood flow (CBF), using the hydrogen clearance technique, and for cerebral levels of the thromboxane metabolite TXB2, and prostaglandins 6-keto-PGF1 alpha and PGE2, as well as the leukotriene LTB4. The gerbils were anesthetized with pentobarbital, and half of the animals were pretreated with the cyclooxygenase inhibitor indomethacin. All received 10 or 20 minutes of dense forebrain ischemia followed by reperfusion of 10 minutes, 50 minutes, or 100 minutes. A separate control group received no ischemic lesion. Regional CBF decreased significantly from 23.7 +/- 2.6 to 4.3 +/- 1.7 cc/100 gm/min during ischemia (p less than 0.01). Reperfusion resulted in initially normal flows (22.5 +/- 5.1 cc/100 gm/min) followed by a progressive hypoperfusion (11.3 +/- 2.7 cc/100 gm/min). All metabolites showed parallel significant (p less than 0.05) increases after transient ischemia and reperfusion compared to baseline levels (values (in pg/mg protein) were: TXB2 45.5 +/- 7.1 vs 23.3 +/- 3.6; 6-keto-PGF1 alpha 262.8 +/- 47.9 vs 175.8 +/- 26.8; PGE2 256.5 +/- 35.6 vs 112.5 +/- 11.2; and LTB4 37.8 +/- 4.6 vs 24.6 +/- 6). These levels were all significantly decreased (p less than 0.05) by pretreatment with indomethacin except for the leukotriene LTB4, which was increased. Transient cerebral ischemia results in a reperfusion abnormality and the local generation of cyclooxygenase products, which are reduced by pretreatment with indomethacin; however, cyclooxygenase inhibition may result in increased substrate availability for the lipoxygenase system. Studies of such an interaction may lead to new understandings of the pharmacological modification of detrimental vascular changes after transient cerebral ischemia.

6-Ketoprostaglandin F1 alpha↗

PubMed1971