Search PubMed⌕ Search

Biomedical subjects

M D Seidman

Publications and source records attributed to M D Seidman.

At least 37 records · Page 2Linked to original sources
PubMed1996

Association of mitochondrial DNA deletions and cochlear pathology: a molecular biologic tool.

The purpose of these experiments was to develop a method of isolation, amplification, and identification of cochlear mitochondrial DNA (mtDNA) from minute quantities of tissue. Additionally, studies were designed to detect mtDNA deletions (mtDNA del) from the cochlea that previously have been amplified from other organ systems and tissues. MtDNA del have been associated with many pathologies, including neurological disorders, sensorineural hearing loss, ischemia, cardiomyopathies, and aging. DNA was extracted from rat and human tissues, and polymerase chain reaction was used to amplify mtDNA sequences. A 360 base pair (bp) cytochrome-b gene product and the highly conserved ND1-16S ribosomal ribonucleic acid regions found only in mtDNA were amplified from all tissues. Preliminary studies have identified a 4834 bp mtDNA del in aged rats and a corresponding 4977 bp mtDNA del in aged humans. Additionally, preliminary results in human archival temporal bone studies reveal the presence of the 4977-bp mtDNA deletion in two out of three patients with presbycusis. The deletion was not evident in age-matched control patients without a history of presbycusis. This technique of mtDNA identification makes it possible to investigate specific mtDNA defects from a single cochlea, promoting the study of hereditary hearing loss and presbycusis at a molecular biologic level.

Aged↗
PubMed1996

Pentoxifylline maintains cochlear microcirculation and attenuates temporary threshold shifts following acoustic overstimulation.

The etiology of noise-induced hearing loss is poorly understood despite years of clinical experience and experimental investigations. One potential mechanism which may contribute to noise-induced temporary threshold shifts (TTS) are vascular pathologies in the microcirculation of the cochlea. Several studies have demonstrated histologic evidence of reduced cochlear blood flow following noise exposure. Recent studies utilizing intravital microscopy (IVM) complement these histologic studies and furthermore demonstrate localized ischemia during noise exposure. The purpose of the current study was to attempt to maintain cochlear blood flow during noise exposure by treating with pentoxifylline, a xanthine derivative which promotes blood flow in capillary beds. The possibility that preserved cochlear microcirculation with pentoxifylline treatment attenuates noise-induced TTS was also examined in this study. The results show treatment with pentoxifylline maintains cochlear microcirculation as assessed by continuous red blood cell movement through capillaries. Pentoxifylline treatment did not prevent vasoconstriction or increased permeability often observed in the cochlear microvasculature during noise. Treatment with this drug reduced noise-induced TTS.

Animals↗
PubMed1996

Update on tinnitus.

The study of a disorder such as tinnitus is fraught with difficulties. Tinnitus, like pain, is a subjective symptom. The problem is compounded because several different mechanisms must operate to cause the persistent sensation of tinnitus. Therefore, it is difficult to measure objectively any improvements in the condition. For example, it has been reported previously that sectioning the eighth cranial nerve does not abolish tinnitus in a majority of patients; therefore, central mechanisms must act to preserve the tinnitus. Finally, we know that tinnitus can occur in a host of conditions other than ototoxicity, aging, and noise exposure. Other conditions that may produce tinnitus are migraine headache with auditory aura, temporal lobe seizures, and head injuries. Therefore, it is naive to conceptualize that tinnitus is a disorder with a unitary origin and a unitary "cure".

Diagnosis, Differential↗
PubMed1995

The jugular dural fold-a helpful skull base landmark to the cranial nerves.

During a retrosigmoid (or combined retrolabyrinthine-retrosigmoid) approach to the posterior fossa for vestibular neurectomy or removal of small acoustic neuromas, a white dural fold is a consistent landmark to cranial nerves VII through XII. This fold of dura appears as a white linear structure extending from the foramen magnum across the sigmoid sinus, attaching to the posterior aspect of the temporal bone, anterior to the vestibular aqueduct. The name "jugular dural fold" is suggested for this landmark. The jugular dural fold overlies the junction of the sigmoid sinus and the jugular foramen. As measured in formalin-fixed cadaver heads, the overall length of the jugular dural fold is 20.8 mm (+/- 2.9 mm). The cochleovestibular nerve lies 9.9 mm (+/- 1.5 mm) anterior to the superior aspect of the jugular dural fold, the glossopharyngeal nerve lies 9.5 mm (+/- 1.6 mm) anterior to the midpoint of the jugular dural fold, and the operculum of the vestibular aqueduct lies 6.6 mm (+/- 0.7 mm) posterior to the jugular dural fold. Intraoperative measurements in patients undergoing combined retrolabyrinthine-retrosigmoid vestibular neurectomy show an overall length of the jugular dural fold of 16.3 mm (+/- 1.9 mm). The cochleovestibular nerve lies 8.6 mm (+/- 1.3 mm) anterior to the superior aspect of the jugular dural fold, the glossopharyngeal nerve lies 8.6 mm (+/- 1.3 mm) anterior to the midpoint of the jugular dural fold, and the operculum lies 7.5 mm (+/- 0.8 mm) posterior to the jugular dural fold. The jugular dural fold can be used as a reliable landmark for rapidly locating cranial nerves in the posterior fossa.

Journal Article↗
PubMed1995

Cochlear vascular changes in response to loud noise.

The findings of several authors suggest that alterations in cochlear vascular physiology may contribute to noise-induced hearing loss. Although the influence of noise on cochlear microcirculation is controversial, recent investigations have identified a number of microvascular alterations during noise exposure. Researchers, using intravital microscopy, a technique which offers the advantage of continuous in vivo observation of cochlear lateral wall vessels, have observed alterations in red blood cell velocity and capillary vasoconstriction within the cochlea during exposure to noise. These alterations were sufficient to induce localized periods of stasis, alterations in vascular permeability, and local ischemia. It is possible that such noise-induced vascular ischemia may result in reduced auditory sensitivity.

Animals↗
PubMed1994

Prediction of facial nerve function following acoustic neuroma resection using intraoperative facial nerve stimulation.

Methods of monitoring the facial nerve during posterior fossa surgery continue to evolve. In an effort to predict acute and final facial nerve function following acoustic neuroma resection, the lowest current applied to the facial nerve at the brainstem necessary to elicit facial muscle response was measured using strain gauge and electromyographic facial nerve monitors. A retrospective analysis of 121 patients who had undergone acoustic neuroma surgery was performed. Sixty-five patients had intraoperative facial nerve monitoring and 44 had sufficient data for inclusion in this study. The acute and final facial nerve functions, according to the House-Brackmann classification, were assessed with regard to intraoperative stimulation-current thresholds. Nineteen of 20 patients who required 0.10 mA or less to elicit a facial muscle response had a House-Brackmann grade I facial nerve outcome. The upper limit of the 95% confidence interval of stimulation threshold for patients with a final grade I facial nerve function is 0.17 mA. All of the patients in this study, with stimulation thresholds ranging up to 0.84 mA, had a final grade III or better result. A poor outcome in our series, a final grade III facial nerve function, is best predicted by a poor acute result, specifically an acute grade VIA facial nerve function. We suggest that it is possible to predict the facial nerve function based on intraoperative threshold testing.

Analysis of Variance↗
PubMed1994

Lipid peroxidation inhibitor attenuates noise-induced temporary threshold shifts.

The purpose of this study was to investigate the protective effects of U74389F (Upjohn Co. Kalamazoo, MI), a 21-aminosteroid/lipid peroxidation inhibitor, and a member of the lazaroid drug class, on temporary threshold shifts in animals exposed to prolonged noise stimulation. Animals treated with U74389F and exposed to noise showed attenuated cochlear action potential threshold (CAP) shifts and cochlear microphonic (CM) when compared to non-drug treated noise-exposed subjects. These data suggest that inhibition of FOR induced lipid peroxidation is an important mechanism in noise-induced asymptotic temporary threshold shifts.

Acoustic Stimulation↗
PubMed1994

Influence of calcitonin-gene related peptide on cochlear blood flow and electrophysiology.

Intra-arterially infused calcitonin gene-related peptide (CGRP) induced dose-dependent decreases in both systemic blood pressure and cochlear blood flow (CBF). However, when subjects were pretreated systemically or locally with the specific receptor antagonist CGRP(8-37), CBF increased, despite decreases in systemic blood pressure in response to CGRP infusions. Micro-infusions of CGRP directly into the supplying arterial network of the cochlea induced dose-dependent increases in CBF that were blocked by CGRP(8-37) pretreatment. Cochlear electrophysiology, as assessed by cochlear action potential and cochlear microphonics, remained unchanged following each condition tested. These results indicate that CGRP is involved in systemic regulation of blood pressure and contributes to the regulation of CBF.

Animals↗
PubMed1993

Substance P increases cochlear blood flow without changing cochlear electrophysiology in rats.

Carotid artery infusions of substance P yielded reductions in systemic blood pressure and elevations in cochlear blood flow (CoBF), measured via laser Doppler flowmeter, with no alterations in cochlear action potentials or cochlear microphonics in Wistar-Kyoto rats. Additionally, direct micro-infusions of substance P into the anterior inferior cerebellar artery, which contributes to the local vascular perfusion of the cochlea, yielded elevations in CoBF with no changes in systemic blood pressure. Pretreatment with a specific substance P receptor antagonist, ([D-Pro2,D-Trp7,9]SP) via the carotid artery or the anterior inferior cerebellar artery, diminished subsequent substance P-induced vascular responses. These results suggest that endogenous substance P, like other vasoactive peptides, may interact with a substance P-specific receptor population in the cochlea and may therefore participate in the ongoing regulation of CoBF. These findings also support the premise that vasodilatory hormones, along with vasoconstrictive agents, may be involved in the autoregulation of CoBF.

Action Potentials↗
PubMed1993

An algorithm for the management of acoustic neuromas regarding age, hearing, tumor size, and symptoms.

An algorithm has evolved for the management of patients with acoustic neuroma. Decisions as to surgery vs. observation, surgical approach, and whether hearing preservation should be attempted depend on age, patient symptoms, size of the tumor, residual hearing, and degree of facial nerve involvement at the time of surgery. Conservative management is used for patients over 65 years of age. This consists of observation or subtotal resection through a translabyrinthine approach, depending on the absence or presence of brainstem signs or symptoms. In patients under 65 years of age, hearing preservation is attempted through the retrosigmoid approach in tumors 1.5 cm or less if pure-tone average is less than 30 dB and the discrimination score is greater than 70%. The translabyrinthine approach is our preferred approach for tumors of any size when hearing is not serviceable. A near-total excision is performed when the facial nerve cannot be separated from the tumor. The rationale for this algorithm in the management of 130 cases of acoustic neuroma over the past 17 years is presented.

Adult↗
PubMed1993

The protective effects of allopurinol and superoxide dismutase on noise-induced cochlear damage.

Several studies have demonstrated that noise exposure may result in local vasoconstriction of cochlear vessels. The subsequent decrease in cochlear blood flow may lead to hypoxia and predispose to the formation of free oxygen radicals (FORs). If hypoxia occurs in response to noise exposure, then drugs that scavenge or block the formation of FORs should protect the cochlea from damage resulting from hypoxic or ischemic events as well as noise trauma. Rats were exposed to 60 hours of continuous broad-band noise (90 dB SPL) and treated with superoxide dismutase-polyethylene glycol (SOD-PEG), allopurinol, or a control vehicle. Exposure to noise resulted in significant threshold shifts at each frequency tested (3, 8, 12, and 18 kHz) as measured by tone burst-evoked compound action potentials and cochlear microphonics recorded from the round window. Both of these thresholds in drug-treated animals were attenuated compared with animals exposed to noise alone. These findings show that SOD-PEG and allopurinol may preserve cochlear sensitivity associated with noise exposure. This suggests that noise-induced damage to the cochlea may be related to the activity of FORs.

Action Potentials↗
PubMed1993

Intraoperative facial nerve monitoring in acoustic neuroma surgery.

Intraoperative facial nerve monitoring simultaneously using electromyography and mechanical pressure sensors is being used in retrosigmoid and translabyrinthine approaches for acoustic neuroma resection. Insulated electrified microsurgical instruments and air drills are used to stimulate the facial nerve with a pulsed, constant current through bone and tumor, before the facial nerve is visually encountered. Electrical stimulation is used to help locate the facial nerve, map the course of the facial nerve within tumor, warn the surgeon of unexpected facial nerve locations, and help predict facial nerve function postoperatively. In 57 unmonitored cases a House-Brackmann (H-B) grade I or II result was obtained in 77 percent of small, 81 percent of medium, and 60 percent of large tumors. In 64 monitored cases H-B grade I or II was obtained in 88 percent of small, 79 percent of medium, and 90 percent of large tumors. Overall, facial nerve outcomes were better after monitored procedures (p < 0.02). A modified H-B classification for acute facial nerve injury is introduced to grade facial weakness immediately postoperatively and until function is stable at 1 year. In the unmonitored group there were five (9%) cases with a complete facial paralysis, facial nerve intact (i.e., acute H-B grade VIA) and seven (13%) cases with the facial nerve transected (i.e., acute H-B grade VIB). In the monitored group there were five (8%) acute H-B grade VIA and two (3%) acute H-B grade VIB results. In the unmonitored group of large tumors, there were statistically more patients with an acute H-B grade VIB result (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The anterior inferior cerebellar arterial network supplying the rat cochlea and its role in autoregulation of cochlear blood flow.

The sensitivity of the cochlea is dependent upon maintenance of a delicate homeostatic environment. One mechanism which participates in providing this environment is the autoregulation of cochlear blood flow. This autoregulation is ensured through the interaction of sympathetic, peptidergic and hemodynamic mechanisms. The current study demonstrates an adaptation that also participates in cochlear blood flow autoregulation. Specifically, an anterior inferior cerebellar arterial network is described and the relative contributions of each of its vessels to total cochlear blood flow is measured using laser Doppler flowmetry. The results show that each collateral vessel contributes to the blood supply of the cochlea and that reperfusion is accompanied by hyperemia. These findings suggest an adaptation that provides stable blood flow through redundancy and compensatory potential. Additionally, these observations have implications for experimental models of ischemia.

Animals↗
PubMed1991

The protective effects of allopurinol and superoxide dismutase-polyethylene glycol on ischemic and reperfusion-induced cochlear damage.

The purpose of this study was to assess the protective effects of allopurinol, a blocker of free oxygen radical (FOR) formation, and superoxide dismutase-polyethylene glycol (SOD-PEG), a scavenger of FORs, on ischemic and reperfusion-induced cochlear damage. Fifteen Wistar Kyoto rats (WKY) were randomly assigned to three groups: (1) a control group (5 animals) that was exposed to 15 minutes of cochlear ischemia by clamping the anterior inferior cerebellar artery (AICA), followed by 15 minutes of reperfusion as documented by laser Doppler flowmetry; (2) a drug-treated group (5 animals) that received allopurinol before ischemia/reperfusion; and (3) a drug-treated group (5 animals) that received SOD-PEG before ischemia/reperfusion. In the control group, the tone burst-evoked compound action potential (CAP) recorded from the round window (RW) of the cochlea was abolished, and the cochlear microphonic (CM) was reduced after ischemia. In contrast, both allopurinol and SOD-PEG-treated animals showed post-reperfusion sensitivity in CAP and CM measures. We interpret these results to indicate that damage to the cochlear from ischemia and subsequent reperfusion can be attenuated by pretreatment with allopurinol or SOD-PEG. This provides indirect evidence that FORs may be partially responsible for cochlear damage resulting from ischemic conditions.

Action Potentials↗
PubMed1991

The protective effects of tirilated mesylate (U74006F) on ischemic and reperfusion-induced cochlear damage.

We have recently demonstrated that allopurinol, a blocker of free oxygen radical (FOR) production, and superoxide dismutase (SOD), a scavenger of FOR, protect the cochlea from damage associated with ischemia/reperfusion. The purpose of this present study was to determine if tirilated mesylate (U74006F), a potent inhibitor of lipid peroxidation, can also protect the cochlea from ischemia/reperfusion. Eleven Wistar-Kyoto rats were randomly assigned to two groups: (1) a control group (6 animals) that was exposed to 15 minutes of cochlear ischemia by clamping the anterior-inferior cerebellar artery (AICA), followed by 15 minutes of reperfusion, and (2) a drug-treated group (5 animals) that received U74006F before ischemia/reperfusion. In the control group, the tone burst-evoked compound action potential (CAP) recorded from the round window (RW) was abolished and cochlear microphonic (CM) was reduced. In contrast, the U74006F-treated animals showed post-reperfusion sensitivity in CAP, and less of a CM threshold shift. We interpret these results to indicate that U74006F lessens cochlear damage occurring as a result of ischemia/reperfusion and supports the hypothesis that FOR-induced lipid peroxidation may be partly responsible for the cochlear damage that occurs from ischemia.

Action Potentials↗
PubMed1990

Angioedema related to angiotensin-converting enzyme inhibitors.

Angioedema is a disorder characterized by well-demarcated nonpitting edema involving the tongue, floor of the mouth, larynx, lips, and face. This condition can progress to upper airway obstruction and death. Angiotensin-converting enzyme inhibitors (ACEIs), relatively new antihypertensive agents, act by blocking the formation of angiotensin II, a potent vasoconstrictor and stimulator of aldosterone formation. ACEIs also retard the breakdown of bradykinin, a potent vasodilator, which may lead to the edema seen in nonhereditary angioedema. These ACEIs include enalapril, captopril, lisinopril, saralasin acetate, and a combination of ACEI with diuretics (for example, Capozide). From August 1987 to January 1989, we treated six patients with a nonhereditary form of angioedema related to ingestion of angiotensin-converting enzyme inhibitors. Symptoms developed in all patients within 12 hours after their initial dose of an ACEI. They presented with shortness of breath and dysphagia associated with tongue and floor of the mouth edema. Two of the six required intubation and monitoring in the surgical intensive care unit for 36 to 48 hours. Three required supportive treatment and observation in an intermediate care unit, and one received supportive care in the clinic and was discharged the same day. Specifically, treatment consisted of cessation of inciting agent, steroids, antihistamines, and epinephrine, if not otherwise contraindicated. Assays of C1 esterase inhibitor levels and C4 were normal in all six patients; this was important in order to rule out hereditary forms of angioedema. These cases will be discussed, including a review of the literature, methods of diagnosis, pathophysiology, and treatment of angioedema.

Aged↗