Hearing loss has been observed in humans and experimental animals in severe vitamin A deficiency. In experimental animals, vitamin A deficiency leads to periosteal bone overgrowth of the internal auditory canal, but atrophy or degeneration of vestibular and cochlear sensory cells does not occur. An analogous situation exists in the sensory cells of the retina; vitamin A deprivation leads to a functional impairment without a histological correlate. Experimental animals maintained with retinoic acid grow and mature normally, but the rods and cones of the retina slowly atrophy. If the sensory cells of the auditory and vestibular apparatus are also vitamin A dependent, degeneration may occur in animals deprived of dietary vitamin A, but supplemented with retinoic acid. To test this hypothesis, weanling rats were fed a diet totally lacking vitamin A but supplemented with retinoic acid. They were killed at intervals and their retinas and inner ears were examined histologically. After 8 months of the above regime, the visual cell nuclei had atrophied. By 12 months, the scala media of the cochlea was filled with an eosinophilic, amorphous substance particularly at the helicotrema. The sensory cells of the cochlea and the vestibular apparatus remained normal in appearance. These findings imply that the tissues of the inner ear depend upon retinol and that retinoic acid does not supply some of the metabolic requirements of the inner ear.

The term "ranula" is poorly understood and is frequently applied to a variety of cystic structures in the head and neck. Ranulas classically are cysts of salivary gland origin, usually the sublingual glands, of which two varieties are described: a simple, epithelial lined cyst resulting from ductal obstruction, and a pseudocyst without epithelial lining resulting from extravasation of saliva that dissects through the tissue planes of the neck and may appear as a neck mass. Four cases are presented that illustrate the difficulties in diagnosis; treatment consists of meticulous dissection of the thin-walled sac in continuity with the excision of the sublingual glands that are the origin of these lesions.

Twenty-five years ago hearing loss was observed in some subjects during a comprehensive study of the effects of hypovitaminosis A on human volunteers. Experimental studies documenting histopathological changes in the temporal bone due to hypovitaminosis A are conflicting. Even the recent textbooks of otolaryngology and physiology make no mention of a role of vitamin A in the ear. To explore the role of vitamin A in the ear adult and weanling rats maintained on a diet totally lacking vitamin A were sacrificed at intervals. Their temporal bones were examined with the light microscope. After six weeks on a vitamin A free diet weanling rats showed hypertrophy of the periostial portions of the otic capsule. At 16 weeks a narrowing of the internal auditory canal due to bony exostoses was present. The neuroepithelia of the cochlea and the vestibular apparatus were histologically normal even in the longest surfiving animals. Adult rats maintained on a vitamin A free diet showed minimal thickening of the bone adjacent to the internal auditory meatus. The cochlea and the vestibular appartus in these animals remained normal throughout the 28-week experiment. Although we have demonstrated marked abnormalities of the otic capsule in hypovitaminosis A, our results do not support those of some earlier investigators who reported that atrophy of the cochlear and vestibular neuroepithelium occurred in the absence of dietary vitamin A.

Five cases of enlogated styloid processes sent in a 12-month period prompted a review of this subject and a reevaluation of the condition as it relates to other neuralgias of the head and neck. We review the head and neck pain syndromes and offer diagnostic criteria that will aid in the differential diagnosis and will facilitate appropriate management.

Six cases of hearing impairment have been presented. Furosemide was administered to all of these patients at the time of the alleged onset of the deafness. None of the known or suspected causes of deafness occurring in transplant patients was evident in these cases. With the experimental evidence that furosemide does induce stria damage and the absence of other recognized causes of deafness in this series of patients, furosemide must be considered the etiologic agent responsible for the permanent sensorineural hearing loss. A characteristic audiometric pattern of hearing impairment emerged and a possible explanation for these features has been given. Certain precautionary steps in the use of ototoxic drugs are suggested.

Several substances are known to have a profound effect on both the kidney and the inner ear. The aminoglycoside antibiotics are toxic to both of these organs. Ethacrinic acid and furosemide affect transport mechanisms in the loop of Henle as well as the inner ear. In addition, studies have suggested antigenic similarities between the stria vascularis of the cochlea and the renal tubules. This report of potassium bromate poisoning and its resultant deafness and renal failure further emphasizes the curious relationship between these two organ systems.

AbstractThe incidence of complications of paranasal sinusitis have been progressively decreasing since the advent of antibiotics. Most of the complications that have occurred are secondary to sub‐acute or chronic sinusitis. A few patients, however, still present with a complication of an acute sinusitis infection. Four cases are presented in detail and 14 cases are summarized which presented with an acute complication as the primary presenting complaint. Sinusitis was not an obvious component in most of these cases, and none of the 18 patients had any previously known sinus disease.The paper was limited to a discussion of complications involving the orbit, the tissues surrounding the sinuses, and the intracranial cavity. Basic information regarding these topics was reviewed.The first case report described a young boy with cellulitis of the orbit and cheek secondary to a maxillary sinusitis. Neither the cellulitis nor the sinusitis responded to the medical treatment until trephine and irrigation of the sinus was performed. The second case report described a young man with a frontal subperiosteal abscess and orbital cellulitis secondary to frontal sinusitis. His treatment consisted of drainage of the abscess and performance of a frontal sinus trephine. The third case described a young man with maxillary, ethmoid and sphenoid sinusitis and a secondary cavernous sinus thrombosis. The maxillary sinuses were drained and the patient was given high doses of intravenous antibiotics and decongestants but he was not anticoagulated. Apart from the central retinal artery thrombosis resulting in the left eye, recovery was complete. The fourth case report described a young lady who had undergone a renal transplant and was maintained on immunosuppressant medications. She developed a meningitis secondary to maxillary sinusitis. Complete recovery occurred on medical treatment alone.The other 14 cases were summarized in a table. These cases were then discussed and recommendations were made regarding management of these complications.It was concluded that with antibiotics in adequate closes, it is now safe to perform a sinus trephine much earlier in the course of the disease than has previously been advocated. Eight of the 18 were drained in the acute phase and there was no evidence of osteomyelitis or other sequella secondary to this procedure. Indeed, six of these patients required surgical drainage before the fever or the complications would respond to therapy. It is suggested that immediate surgical drainage and irrigation is indicated when sinusitis does not respond or becomes clinically worse after 24‐48 hours of treatment with systemic antibiotics and decongestants; or when acute suppurative local infection or septic intracranial complications are present. The sinuses should be irrigated frequently with saline until the return remains clear for 48 hours.The majority of the organisms isolated were staphylococci, coagulase negative and coagulase positive. Four cultures grew no organisms but since routine cultures for anaerobic organisms were not performed these could not be eliminated as a factor in the infection. The majority of cases were treated with high doses of intravenous antibiotics and these were only given intramuscularly 24 to 48 hours after the fever had subsided and the clinical symptoms were resolving. The total duration of antibiotic treatment varied considerably within this series. It is recommended that complicated acute sinusitis should be treated as though an osteomyelitis is actually present. The systemic antibiotics should be continued for a full week after fever disappears before changing to oral antibiotics. The total duration of antibiotic therapy should be for four to six weeks.In treating meningitis, high doses of broad spectrum antibiotics were used until culture sensitivities were available. Examination of cerebrospinal fluid was emphasized. On adequate treatment the C.S.F. sugar levels should rise above the initial values and no demonstrable micro‐organism should be present after 24 hours.It was noted that intracranial abscesses can occur with minimal symptoms and that fever is not necessarily present. If any doubt exists an arteriogram or other investigations should be performed.