The otolaryngologist and tetanus.
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Biomedical subjects
Publications and source records attributed to R L Hilsinger.
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In a prospective study of 1507 patients, evaluated consecutively for facial palsy in the Cranial Nerve Research Clinic at the Kaiser Permanente Medical Center, Oakland, California, between 1966 and 1976, 185 cases (12%) were diagnosed as Ramsay Hunt syndrome. In 46 cases (25%), the diagnosis of herpes zoster was confirmed by acute and convalescent serum titers for varicella-zoster virus. In 139 cases (75%), viral titers were not performed and the diagnosis was based on the characteristic clinical presentation of the Ramsay Hunt syndrome. The data were subjected to multivariate analysis evaluating age, sex, race, signs, and symptoms at onset, severity of paralysis, associated medical problems with concomitant neurologic deficits, and response to therapy. These were compared with data of 1202 patients with Bell's (herpes simplex) palsy. The facial palsy of Ramsay Hunt syndrome was found to be more severe, to cause late neural denervation, and to have a less favorable recovery profile than Bell's (herpes simplex) facial palsy. Prognostic factors and treatment recommendations are discussed.
Bilateral chylothorax is a rare complication occurring after head and neck surgery, with only six cases reported. The diagnosis is not difficult if a high index of suspicion is held. Early recognition and treatment prevent the devastating metabolic effects of excessive chyle loss and reduce the respiratory restriction that can progress to fatal anoxia. Dietary management with medium-chain triglycerides is essential to successful outcome. Repeated invasive therapy should be minimized.
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In the past, most cases of facial paralysis have been erroneously labeled Bell's palsy. Bell's palsy has been synonymous with and defined as idiopathic facial paralysis affecting only the facial nerve within the confines of the temporal bone. In the last ten years, Bell's palsy has been redefined as viral polyneuritis, probably caused by herpes simplex reactivation, and its diagnosis is no longer reached by exclusion. This article discusses the signs, symptoms, and testing necessary to confidently and accurately differentiate Bell's palsy from other forms of facial paralysis. The nonspecificity of topographic diagnosis is discussed and statistical analysis of factors affecting prognosis are included.
The treatment of facial paralysis requires a reliable estimate of prognosis as well as an accurate diagnosis. Although the majority of patients recover, the degree of subsequent facial function varies. An estimation of the risk of nerve degeneration and subsequent disability is needed to guide therapy and to advise patients. Currently, prognosis is obtained by clinical evaluation of initial signs and symptoms, specific nerve excitability and function testing, and response to medical therapy. This study attempts to identify and quantitate factors that predict the outcome of facial paralysis. In 1214 patients with Bell's palsy, we identified factors associated with a severe course or poor outcome. We analyzed the predictive value of each item in an extensive research protocol, estimating the relative contribution to the total risk of unfavorable outcome by means of multiple regression models. With the use of these data, we have developed the facial paralysis prognostic index (FPPI). The FPPI can assist otologists to more accurately estimate outcome based on physical examination and electrical testing.
Although the TMJ or myofascial pain-dysfunction syndrome is probably not brought about by any single etiologic agent, the findings discussed here offer strong evidence that the primary disease is a form of cranial polyneuritis similar in onset, duration, and natural course to acute facial paralysis. These findings of sensory neuritis with secondary neuromuscular dysfunction leave no question unanswered, whereas the classic concept that has evolved through the years into the pain-dysfunction syndrome cannot adequately explain the myriad of signs and symptoms found in this condition. By removing the psychophysiologic (functional) label and recognizing the organic nature of this self-limiting disease, we should now be able to consolidate the many different modes of therapy that are effective in treating patients with the acute TMJ pain-dysfunction syndrome.
Vestibular vertigo traditionally has been considered to be of viral origin and some forms (acute vestibular neuronitis, acute labyrinthitis, acute vertigo) may be manifestations of a viral cranial polyneuritis. To test this hypothesis, otoneurologic signs and serum complement-fixation titers to herpes simplex and herpes zoster were determined in 16 patients with acute vertigo during their attack and several weeks later. One hundred unselected patients seen for nonotoneurologic problems served as control subjects. In addition to vestibular nerve abnormality, all patients with vertigo had some form of cranial nerve abnormality that cleared within four weeks of onset. These transient acute cranial nerve findings in patients with vestibular vertigo support the concept of inflammatory polyneuritis, and preliminary studies indicate that an anti-inflammatory agent such as prednisone may be the preferred treatment.
Although endolymphatic hydrops is generally considered to be the most prominent factor in the etiology and pathology of Ménière's disease, we have concluded that this condition more probably represents a polyganglionitis caused by the herpes simplex virus with secondary hydrops changes. The wide range of symptoms occurring in the Ménière's disease complex is illustrated in seven selected cases which support this conclusion. Vestibular nerve section can stabilize hearing and relieve episodic vertigo by removing the locus of viral infection and precluding recurrent activation.
In a series of 1502 patients seen in our Facial Paralysis Research Clinic 1048 were diagnosed as having Bell's palsy. Review of clinical, epidemiologic, and laboratory data, plus review of the literature, has led to the conclusion that Bell's palsy is an acute benign cranial polyneuritis probably caused by reactivation of the herpes-simplex virus, and the dysfunction of the motor cranial nerves (V, VII, X) may represent inflammation and demyelinization rather than ischemic compression. Spinal fluid analysis suggests that the disease is a phenomenon of the central nervous system with secondary peripheral neural manifestations. With our presently available information, treatment of a viral disease with an anti-inflammatory agent is rational. Prednisone treatment started within the first week of the disease can restore better function to the paralyzed face than is achieved without such therapy, and facial nerve decompression has been unnecessary.
Sera from all 41 adult patients with idiopathic facil paralysis (Bell palsy) and 35 (85%) of 41 matched controls who had never had Bell palsy contained antibodies to herpes simplex virus (P smaller than.05). The frequency of antibodies to herpes zoster virus did not differ in patients and controls. A rise in antibody titer, indicating primary herpes simplex virus infection, was not found in these patients. That Bell palsy may be caused by reactivation of herpes simplex virus is suggested by (1) clinical, neurologic, laboratory, and immunologic similarities between idiopathic facial paralysis and known manifestations of reactivated herpes simplex virus infection, and (2) the known neurotropism of herpes simplex virus, including its presence in latent form in the trigeminal ganglia, and parallels with known facial paralysis due to varicella zoster virus, a closely related agent. The presence of antibodies to herpes simplex virus is the only common factor among the patients tested in this study.
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The records of 42 women with Bell's palsy during pregnancy, and of 91 nonpregnant women, whose dats of onset of Bell's palsy and of the preceding menstrual cycle were precisely known, were studied for factors that might show relation between pregnancy or the menstrual cycle and Bell's palsy. Of the 42 cases in pregnancy, 31 occurred in the third trimester, five in the first two weeks postpartum, and six in the first two trimesters combined. Our calculated frequency of Bell's palsy in pregnant women is 45.1/100,000 births; for nonpregnant women of the same age group the calculated incidence is 17.4/100,000 per year. No causative relation was found between toxemia, hypertension or primigravidity, and Bell's palsy. Over 60% of the cases in nonpregnant women occurred in the first 14 days of the menstrual cycle with peaks on the first and seventh days and near ovulation. No clear evidence for an etiologic relationship was seen with edema or hormonal changes in either pregnancy or the menstrual cycle. A number of factors in pregnancy and the menstrual cycle suggested an etiologic role for herpes simplex virus reactivation in Bell's palsy. There was no evidence that prednisone treatment is contraindicated during pregnancy.
Narrowing of the intrathoracic trachea in the coronal plane with anteroposterior lengthening is characteristic of the "saber-sheath" trachea deformity. This structural disorder is strongly associated with chronic obstructive pulmonary disease and may be related to chronic bronchitis. Although lateral compression suggests weakening and collapse, the supporting tracheal cartilage is usually thickened and densely calcified. We present a patient who was discharged after uneventful total laryngectomy but later complained of increasing airway obstruction from crusted secretions, resulting in visits to the emergency room and admission to the hospital. After the diagnosis was made by computed tomography, tracheal dilation was performed with some improvement. The diagnostic findings of the saber-sheath trachea, differential diagnosis, possible causes, and clinical implications are discussed.
Evidence suggests that many cranial nerve syndromes, such as migraine headache, acute vestibular neuronitis, globus hystericus, carotidynia, acute facial paralysis (Bell's palsy), and Meniere's disease, are caused by the neurotropic herpes simplex virus (HSV). Because transitory cranial nerve dysfunction during acute HSV infection can be asymptomatic but often occurs in conjunction with mucocutaneous vesicles, we tested five subjects with herpes labialis for cranial nerve dysfunction. Four of the subjects had hypesthesia of the trigeminal nerve (which recurred in two); four, hypesthesia of the glossopharyngeal nerve; and two, hypesthesia of the second cervical nerve. Three of the subjects had positional or spontaneous nystagmus (which recurred in one); one of the subjects had a unilateral, decreased caloric response of 50%. Unilateral weakness of the cricothyroid muscle or the palate occurred in three of the subjects (and recurred in one). Volitional electromyograms were normal in all the subjects, but two of the subjects had increased facial nerve latency (which recurred in one). Similar findings of an acute, transitory nature should suggest to the clinician a viral polyganglionitis caused by HSV infection.
Acute superior laryngeal palsy is often clinically unrecognized and frequently overlooked. Yet, this motor paralysis occurs more frequently than facial paralysis. Like acute facial paralysis, superior laryngeal palsy often occurs as part of a cranial polyneuritis that is probably related to herpes simplex virus reactivation. Rotation of the larynx and shortening of one vocal cord have been found in such diverse syndromes as vestibular neuronitis, migraine and tension headaches, unexplained cough, tinnitus aurium, globus hystericus, and carotidynia. Electromyographic studies suggest that laryngeal spasm may be caused by faulty regeneration of the superior, rather than the recurrent, laryngeal nerve.