Biomedical subjects
Publications and source records attributed to T P Murphy.
Rhinorrhea after neurotologic surgery may be indicative of a cerebrospinal fluid (CSF) leak or may be secondary to autonomic dysfunction as a result of injury to preganglionic parasympathetic fibers. Differentiation between these two conditions is essential because undetected CSF rhinorrhea may lead to meningitis and death.
Bilateral facial paralysis is a diagnostic challenge, which may manifest itself as either a simultaneous or alternating form, occurring in 0.3-2.0% of patients that present with facial paralysis. The differential diagnosis of facial paralysis includes congenital, traumatic, neurologic, infectious, metabolic, neoplastic, toxic, iatrogenic and idiopathic etiologies. While idiopathic facial paralysis is the most common diagnosis, a comprehensive evaluation must be completed prior to this diagnosis in patients with bilateral facial paralysis. A representative case of simultaneous bilateral facial paralysis is presented. The literature is reviewed and discussed. A diagnostic protocol for the evaluation of bilateral facial paralysis is proposed. Bilateral facial paralysis requires a thorough evaluation and may prove to be a diagnostic dilemma.
Using a monoclonal antibody (mAb), designated AMP1, a novel cell adhesion molecule was identified on rat astrocytes and oligodendrocytes. When confluent monolayers of cultured rat astrocytes were labeled with AMP1, the antigen was discretely localized to the cell surface in regions of cell-cell contacts. The antibody did not label embryonic rat cortical neurons plated on monolayers of neonatal astrocytes, indicating that the antigen is neither present on cultured neurons nor does it reorganize on the glial surface under the neurons. On immunoblots of astrocytic or brain proteins, mAb AMP1 recognized a 106 kDa protein. In the present paper, data are presented demonstrating that the AMP1 antigen is a cell adhesion molecule and is distinct from all the known cell adhesion molecules present on astrocytes: N-CAM, N-cadherin, or members of the beta 1 integrin family. We have tentatively termed this molecule 'glial cell adhesion molecule' (G-CAM).
The signals required to induce S phase entry in murine splenic B cells were found to be altered by prolonged treatment with low doses of anti-Ig antibody. Whereas fresh splenic B cells are stimulated by the combination of a phorbol ester protein kinase C agonist plus a calcium ionophore, anti-Ig-treated splenic B cells were stimulated by phorbol ester alone, in the absence of a comitogen. The majority of these phorbol ester responsive B cells expressed CD5. The phorbol ester responses of anti-Ig-treated splenic B cells paralleled those previously reported for untreated peritoneal CD5+ B cells in a number of respects: responses were not idiosyncratic to phorbol esters but occurred with nonphorbol protein kinase C agonists; phorbol ester responses were enhanced by IL-4; and, phorbol ester responses occurred rapidly and were greater at 24 than at 48 h. However, the effect of agents that act to raise intracellular levels of cAMP distinguished between anti-Ig-treated splenic B cells and untreated peritoneal B cells in that the phorbol ester responses of the former were enhanced whereas the responses of the latter were inhibited. The present results add a functional dimension to the phenotypic similarity between splenic B cells treated with anti-Ig and resident peritoneal B cells that constitutively express CD5; however, some differences in behavior were noted.
One hundred one LG-Medical (LGM) vena cava filters were placed in 97 patients at four institutions. Placement was a complete technical success in 90% (91 of 101). In 6% of attempts, LGM filter insertion was complicated by incomplete opening of the filter. Pulmonary embolism after filter placement was not definitely demonstrated in any patient. The probability of inferior vena cava patency was 92% at 6 months after filter insertion. Thrombosis at the insertion site was seen in eight of 35 patients (23%) evaluated with duplex ultrasound or venography. Thrombus was observed in 37% of filters at follow-up examination, with cephalic extension of thrombus above the filter in 20% of all patients examined. Filter migration (greater than 1 cm) was seen in 12%; significant angulation was observed in only one patient (2%). In vitro experimentation demonstrated that incomplete opening of the LGM filter during placement can be avoided, in part, by brisk retraction of the insertion cannula. The low-profile introducer system of the LGM filter allows increased alternatives in selecting the site for filter insertion. The low-profile system also makes outpatient filter placement a possibility. No significant difference in the prevalence of thrombosis at the insertion site following LGM filter insertion was noted compared with previous results reported for percutaneous transfemoral placement of the Greenfield filter. The nonopaque sheath does not permit careful localization prior to filter deposition. Modification of the LGM filter to include a radiopaque sheath is suggested.
Gadolinium-enhanced MRI was used to evaluate 10 patients with Bell's palsy and one patient with facial paralysis secondary to Lyme disease. Nine of the eleven patients showed increased signal intensity of their facial nerve with gadolinium-enhanced MRI. In all nine patients, the facial nerve was involved at the labyrinthine, geniculate ganglion and proximal tympanic portions of the facial nerve, while two of the nine patients also had involvement of the mastoid segment of the facial nerve. Patients whose facial nerve enhancement was limited to the labyrinthine, geniculate ganglion and proximal tympanic facial nerve ultimately had complete return of facial function. Patients whose facial nerve enhanced in the mastoid segment experienced incomplete return of facial function. Gadolinium is effective in localizing the site of inflammation during facial paralysis. Those patients with enhancement localized to the labyrinthine, geniculate ganglion and proximal tympanic segments were more likely to regain complete facial function. In contrast, patients who had enhancement of the mastoid segment of the facial nerve had poorer prognoses for complete return of facial function.
Explore the source record for details and available documents.
Twenty-five patients with Bell's palsy were evaluated to assess the efficacy of gadolinium (Gd+)-enhanced MRI in determining: (1) the site of facial nerve enhancement, (2) the relationship between EMG findings and Gd+ MRIs, and (3) the usefulness of Gd+ MRI in predicting recovery of facial function. Eighteen of twenty-five patients had enhancement of the facial nerve during Gd+ MRI whereas seven did not. The most common areas of facial nerve enhancement were the labyrinthine, geniculate ganglion, and proximal tympanic segments of the facial nerve. EMGs were performed on ten patients who lost nerve excitability. The segments of facial nerve enhanced during Gd+ MRI varied in location and intensity in patients who maintained nerve excitability and in patients who lost nerve excitability. There was no correlation between EMG findings and location of facial nerve enhancement in patients who lost nerve excitability. The location of facial nerve enhancement during Gd+ MRI was not useful in predicting recovery of facial paralysis.
Otologic manifestations of pseudotumor cerebri heightened awareness of pseudotumor cerebri and its varied subtle presentations will allow for a more expedient diagnosis by the otolaryngologist. Pseudotumor cerebri is defined as increased intracranial pressure and papilledema without a mass lesion or obstruction of the ventricular system. Presenting symptoms most commonly are headache and visual dysfunction. However, patients may present with associated symptoms of tinnitus, dizziness and hearing loss. These patients may be seen first by the otolaryngologist. Fourteen patients with a diagnosis of pseudotumor cerebri are reviewed. Nine of the 14 patients had neurotologic symptoms during the course of their evaluation. Pseudotumor cerebri is a diagnostic challenge. Keys to diagnosis are a high index of suspicion, careful history and funduscopic examination in patients with unexplained neuro-otologic symptoms.
Sensorineural hearing loss (SNHL) has many etiologies including vascular sources. Vascular causes of SNHL can occur at the microvascular level. Macrovascular level may be described as arising from vessels proximal to the labyrinthine artery or those vessels that can be visualized without the aid of a microscope. Otologic symptomatology and diagnostic evaluation of the SNHL may reveal a macroscopic vascular source. Representative cases of macrovascular sensorineural hearing loss due to aneurysm, arteriovenous malformation, and vertebrobasilar artery dolichoectasia are presented.
B cell expression of the surface glycoprotein, Pgp-1 (Ly-24), was evaluated using flow cytometric analysis. Pgp-1 expression on naive, conventional (splenic) B cells was low but could be increased by mitogenic stimulation. Pgp-1 expression on naive peritoneal B cells was higher than expression by unmanipulated conventional B cells, suggesting the possibility that peritoneal B cells have been activated in vivo. However, the elevated expression of Pgp-1 by peritoneal B cells was not accompanied by increased expression of surface Ia but was correlated with Ly-1 status. Further, Pgp-1 expression by B cells from germ-free mice did not differ from that of normal animals. The elevated expression of Pgp-1 by peritoneal B cells is superficially similar to that provoked by mitogenic stimulation of conventional B cells; however, several characteristics suggest that the elevated expression of Pgp-1 by peritoneal B cells does not reflect prior activation of these cells.
We report a case of delayed diagnosis of a fracture dislocation of the base of the fifth metacarpal with a resultant ulnar motor nerve lesion. The patient achieved marked improvement after fracture reduction and ulnar neurolysis.
Forty-six patients with a diagnosis of acute deep venous thrombosis (DVT) established by means of duplex ultrasound (US) were prospectively followed up with serial duplex US examinations during a 6-month period to assess the persistence of venous abnormalities. All patients were asymptomatic. Isolated popliteal DVT was found to be more likely to revert to normal at duplex compression US than thrombosis involving both the femoral and popliteal systems (P less than .05). Increased venous diameter was a sign of acute clot (P less than .005). Clot echogenicity did not help to enable distinction of acute DVT and chronic DVT. At compression US, 10 of 21 patients (48%) who initially had occlusive thrombosis had persistent abnormalities that mimicked findings consistent with acute DVT. Chronic venous changes that persisted after 6 months consisted of either lumen recanalization (with resultant intimal thickening) or persistent venous occlusion. Both of these conditions can result in incomplete compression, the major US indication of acute DVT. This appearance should not be confused with that of acute DVT. Follow-up examinations to establish a baseline appearance can be obtained as early as 6 months after an acute episode of DVT.
We investigated whether exposure of guinea pig tracheal tissue to hypochlorous acid (HOCl) or hydrogen peroxide (H2O2) by perfusion through the airway lumen affected the responsiveness of airway muscle to ACh, KCl, or substance P in the presence or absence of 1 microM phosphoramidon, an inhibitor of neutral endopeptidase (NEP). Pairs of tracheal segments were immersed in a Krebs solution (pH 7.40 at 37 degrees C) and connected to perfusion circuits so that the lumen of one segment of each pair could be perfused with Krebs solution while the other was perfused for the same time (10 min) with either 0.1 microM HOCl or 10 mM H2O2. Segments after perfusion were cut into rings of similar size and placed in muscle chambers so that airway muscle force generation in vitro could be measured on stimulation by cumulative agonist doses. In addition, cell homogenates were made from other, similarly perfused tracheal segments to assess NEP activity using reverse-phase, high-pressure liquid chromatography (HPLC). We found that smooth muscle of mucosa-intact guinea pig airways perfused with HOCl, but not H2O2, was hyperresponsive to substance P but not to ACh or KCl. HOCl-perfused rings were not different from Krebs solution-exposed rings pretreated with phosphoramidon. There was no increase in substance P responsiveness of HOCl-exposed airways in which the mucosa had been removed before testing in vitro. The substance P hyperresponsiveness of HOCl-exposed, mucosa-intact airways was associated with decreased NEP activity.(ABSTRACT TRUNCATED AT 250 WORDS)
We investigated the effects of ozone exposure (3.0 ppm, 2 h) on the responsiveness of guinea pig airway muscle in vitro from animals developing bronchial hyperreactivity. Muscarinic reactivity in vivo was determined by measuring specific airway resistance (sRaw) in response to increasing concentrations of aerosolized acetylcholine (ACh) administered before and 30 min after exposure. Immediately after reactivity testing, multiple tracheal rings from ozone- and air-exposed animals were prepared and the contractile responses to increasing concentrations of substance P, ACh, or KCl were assessed in the presence of 10 microM indomethacin with or without 1 microM phosphoramidon, an inhibitor of neutral endopeptidase. Isometric force generation in vitro was measured on stimulation by cumulative concentrations of the agonists, and force generation (in g/cm2) was calculated after determination of muscle cross-sectional area. The smooth muscle of mucosa-intact airways from guinea pigs with ozone-induced bronchial hyper-reactivity proved to be hyperresponsive in vitro to substance P and ACh but not to KCl. Pretreatment with phosphoramidon abolished the increase in substance P responsiveness but had no effect on muscarinic hyperresponsiveness after ozone exposure. Furthermore, substance P responsiveness was not augmented in ozone-exposed airways in which the mucosa had been removed before testing in vitro. Likewise, muscarinic hyperresponsiveness was not present in ozone-exposed airways without mucosa. Our data indicate that airway smooth muscle responsiveness is increased in guinea pigs with ozone-induced bronchial hyperreactivity and suggest that this hyperresponsiveness may be linked to non-cyclooxygenase mucosa-derived factors.
In this prospective study the authors attempted to determine the effect of lung resection for bronchogenic carcinoma on final pulmonary function in patients who had severe limitation of lung air flow preoperatively and were therefore likely to have severe, progressive pulmonary failure and in those who had acceptable pulmonary function preoperatively. Preoperative and postoperative pulmonary function tests were performed on 20 patients chosen to undergo various types of resection for bronchogenic carcinoma. Those who underwent pneumonectomy had changes in lung volume that were expected for a resection of that magnitude. Patients who underwent lesser resections had more variable postoperative lung volumes and flows. The patients whose preoperative pulmonary function was poorest had the least change postoperatively and even, in some cases, showed some improvement in function, yet they were the ones most likely to be denied surgery, because of their poor preoperative pulmonary function.
The charts of 35 patients were reviewed retrospectively to determine the effects of embolization on glomus jugulare tumors. Eighteen patients underwent embolization; 17 did not. All tumors were removed with a type A infratemporal fossa approach. The charts were evaluated for operative blood loss, operative time, length of hospitalization, new postoperative cranial nerve deficits and recurrence of tumor. Embolized patients had significantly less operative blood loss and operative time. Embolization did not affect length of hospitalization or reduce the incidence of new postoperative cranial nerve deficits. The surgeon's experience also plays a central role in reducing operative blood loss and operative time. The potential risks of embolization must be considered in the treatment regimen of glomus jugulare tumors.
A 58-year-old man with severe left lower extremity claudication and rest pain underwent percutaneous transluminal angioplasty. A high-pressure balloon was inflated in an area of severe atherosclerotic narrowing. The patient complained of severe pain during inflation and had a vasovagal response. After balloon deflation, angiography displayed extravasation just inferior to the lower edge of the balloon. Immediate inflation of the balloon tamponaded the leak and allowed the patient's transfer to the operating room in stable condition. It is hypothesized that the new high-pressure balloons can overcome resistance in nondistensible arterial walls, causing rupture without balloon rupture.