be carefully prepared and rendered as far as possible aseptic beforehand, and it is safer to inject cold solid paraffin than in the liquefied state.

But many operators inject the paraffin liquefied by warming. Downie always melts it and uses a special needle heated by an electric current to keep the paraffin melted, as the wax cools so quickly that there is always a tendency for it to solidify as it runs down the needle. Harmon Smith till recently used paraffin with a melting-point of 110° F. introduced while liquefied. Gersuny, who originally introduced the method, uses a wax with a melting point of 35°-40° C., which at ordinary temperature is of about the consistency of butter, and he prefers this to either harder or softer varieties, and it does not require to be heated before using.

If Gersuny's soft wax or a wax liquefied by heat is used, an ordinary hypodermic syringe may be employed, or by preference Downie's or Lake's syringe, which tend to keep the wax liquid in the needle; but if introduced in the solid state, Mahu's, Killian's, or Pfau's syringe, or some such specially devised syringe, is necessary. I generally use Mahu's syringe, with wax of a melting-point of 115° F. injected cold, as I think it is probably safer than the liquefied paraffins.

The needle must be directed from above downwards and made to puncture the skin near the mid-line, the point being pushed subcutaneously to the centre of the most depressed area. The injected paraffin should be moulded by the operator's fingers as soon as it enters the tissues. Only small quantities should be introduced at any one time; care is required on the side of injecting too little rather than too much, as it is always easy to inject more after sufficient time has elapsed to allow the tissues to regain their normal state; but it is very difficult indeed to remove any excess after injection. Moreover, if too much is introduced at one time there is an increased risk of the surrounding tissues being irritated, or suppuration, and migration is sometimes attributable to too much paraffin being injected. under undue pressure.

During injection the root and sides of the nose should be firmly compressed by the fingers of an assistant, so that none of the injected substance can escape upwards on the forehead or laterally to the eyelids.

When sufficient paraffin has been injected, a stream of cold water should be poured over the surface of the region involved to ensure

the paraffin setting before withdrawing the needle, and thus obviate the escape of any paraffin through the track of the needle, the puncture being closed with collodion or celloidin.

Cicatrices make it difficult or impossible to introduce paraffin and retain it at the right spot unless they are raised by a tenotomy knife two days before the paraffin is injected.

Harmon Smith advises that no syphilitic, diabetic, or nephritic patient should be injected without due consideration.

Rhinophyma or Fibrolipoma Nasi.-Lipoma is a less common form of growth on the exterior of the nose than it is intranasally, and generally is largely composed of fibrous tissue, forming more or less pendulous masses growing from the alar regions and the lower end of the nose, a condition termed rhinophyma. When these give rise to disfigurement sufficient to call for treatment, the deforming mass should be shaved off, for it is seldom possible and never necessary to save the skin. One should avoid removing too much so that, when the bared surface epitheliases over, the normal contour of the nose is preserved.

ANOSMIA and Hyposmia. For clinical convenience it is usual to include under the terms anosmia, persistent loss of smell, and hyposmia, partial loss, from whatever cause, whether due to local conditions of the mucous membrane or to impairment of the peripheral or central nerve structures. For the proper perception of odours it is essential that the odoriferous particles be able to reach the mucous membrane of the upper part of the nasal passages, and that these should be in a moist condition. Therefore any local affections preventing respiration through the nasal passages, or deposits of mucus and secretion on the olfactory mucous membrane, or a permanently dry condition of the membrane, will interfere with or completely abrogate the sense of smell. Acute and chronic catarrh, and mucous polypi, are common causes of anosmia.

Anosmia may result from congenital absence of pigment in olfactory nerve cells, as in albinos, or from the terminal filaments of the olfactory nerves being altered or impaired, either from a chronic local inflammatory affection, or from atrophic rhinitis, or as the result of injecting very irritating sprays or douches. Injuries to the nerves from blows, fractures of the cribriform plate, peripheral neuritis in infectious diseases, particularly influenza, are among the peripheral causes of anosmia.

Central nerve lesions may cause anosmia; thus it may occur in

hysteria, locomotor ataxia, general paralysis, or from basilar meningitis, syphilis, aneurysms, and exostoses affecting the olfactory bulbs. Intracranial tumours implicating the olfactory lobes and growths destroying the cortical centres for olfaction or their nerve fibres to the lobes, particularly lesions of the horn of Ammon, the hippocampus and the island of Reil (Lermoyez) are other causes, but it is only very rarely that tumours or intracranial hæmorrhages produce anosmia, as it is unlikely that both bulbs would be destroyed. A few cases of unilateral anosmia, hemianosmia, in hysteria and from unilateral destruction of the olfactory bulb, are recorded.

Reflex anosmia has been observed to follow removal of both ovaries. The term "essential anosmia " has been applied to cases in which no local cause or lesion whatever is present to cause it. It is then usually associated with anesthesia of the nasal mucosa.

Hyperosmia.-Increased sensitiveness to smell is sometimes found. in hysteria, neurasthenia, and hypochondriasis, or it may be due to irritation of the olfactory lobes from various causes.

Parosmia, or perversion of the sense of smell with imaginary or subjective perception of odours, is nearly always central, and may occur in hysteria, hypochondriasis, in epileptics, in lesions of the anterior lobes, and in insanity.

Cacosmia, the perception of a bad odour, though generally objective and due to a foreign body in the nose or to accessory sinus disease, may be subjective, and either functional or due to central nerve disease, e.g., cacosmia in nasal crises of tabes.

Patients with unilateral anosmia do not generally perceive the loss of power of smell, and when it is bilateral they mostly complain of loss of taste. In testing the sense of smell it is important to use an odoriferous substance which is non-irritating to the nerves of ordinary sensation, and some well-known smell, such as musk, rose, etc.

Prognosis in anosmia depends (a) on the nature of the lesion, and (b) on its duration. When due to some cause which can be removed, such as polypi, or to hysteria or to peripheral neuritis, the prognosis is favourable provided it has not persisted for a long time. But when the cause is some central lesion or a destructive local lesion, recovery is improbable.

Treatment consists in the removal of the local cause when possible. Local injections of strychnine, local galvanization, the administration of arsenic and strychnine, and general treatment of any neurosis are the most that can be done.

We have already noted the anatomical association of the nasal nerve supply (see p. 34) with the vagus nuclei in the bulb and with the sympathetic, and there is ample evidence also of a close relationship between the nasal passages and the sexual organs, to which fuller reference will be made; hence a number of affections are instances of true nasal neuroses. Nevertheless, it is important to avoid referring neuroses to a nasal source whenever it is possible to detect some slight anatomical defect in the nose or to excite a physiological reflex in response to local irritation by a probe. Each case in which an intranasal cause for an existing neurosis is suspected must be judged on its merits, and, without unduly underestimating any local lesion, it is well to bear in mind that the victim of neuroses of any kind is apt to lead the unwary practitioner astray and to build high hopes on the supposed discovery of the cause of his protean malady, often ending in bitter disappointment.

On the other hand, in many cases which at first sight appear to be pure neuroses, further careful search will reveal an adequate local cause for the condition of the patient, the removal of which will alone effect relief. Indeed, inasmuch as the nasal mucosa is a highly sensitive area which is in health the region for excitation of numerous physiological reflexes, it is inevitable that correlated reflex areas should sometimes be pathologically excited through the nose, in accordance with the law of irradiation of reflex action, viz., that reflex action extends from nervous areas in which it first operated to neighbouring efferent nerve areas by means of the communications between the different groups of ganglionic nerve cells.

Thus reflex nasal neuroses most frequently excite physiological reflexes and other symptoms in the upper respiratory tract-e.g., sneezing, coryza and vascular turgescence; next in frequency, morbid reflex phenomena in the lower tract—e.g., asthma, vasomotor bronchitis, while only very rarely are epilepsy, melancholia, cardiac symptoms, etc., dependent on nasal sources.

Hyperæsthesia is generally the immediate local factor in nasal cough, paroxysmal sneezing, hay fever, and hay asthma, but in all these conditions it is usual to find more or less definite abnormal conditions of the nasal mucous membrane associated with hyperæsthesia in the nasal passages.