Edward C. Clark

Neurologic signs and symptoms as early manifestations of systemic lupus erythematosus.

ALTHOUGH systemic lupus erythematosus is a generalized disease, in the course of which neurologic symptoms or signs might be expected to occur, it has been only within recent years that the neurologic aspects have elicited much interest. In general, it has also been felt that evidence of neurologic dysfunction usually is a late accompaniment, seen only in the terminal stages of this disease. Very little has been written concerning neurologic symptoms or signs occurring early in the course of systemic lupus erythematosus. In recent years several patients with systemic lupus erythematosus have been observed in whom neurologic abnormalities had developed prior to the time that the diagnosis of lupus erythematosus was established. Because neurologic difficulties actually may be among the first, rather than later, manifestations of systemic lupus erythematosus, it seemed of value to present the following three cases. Case 1.-A 16 year old girl was admitted in May 1949 because of left hemiplegia, fever, and pain in the chest. Four years before admission she had had swollen and painful joints and a choreiform movement disorder. The diagnosis of “rheumntic fever with Sydenham’s chorea” had been made. Two years prior to admission she had begun to experience dizzy spells. On one occasion she had had diplopia. At that time she also had a febrile illness, during which left hemiplegia suddenly developed and never abated. The cerebrospinal fluid and results of a pneumoencephalogram were said to have been normal. The sedimentation rate apparently was elevated. Dysarthria and an eruption on the face occurred six months before admission of the patient. The lesions of the face soon became purpuric and thoracic pain began. Aspiration revealed pleural effusion. At admission the patient was found to be acutely ill and drowsy. The blwd pressure was 130/90; pulse rate was 120 per minute; and temperature was 101” F. A fading petechial eruption was present on the trunk, and an erythematous, petechial eruption was seen on the face. Bilateral pleural effusion was noted. The left limbs were spastic and paralyzed. Some weakness of the right limbs also was present. A faint corneal haze was noted. The optic disks were elevated 1 to 2 diopters. Since the adjacent part of the retina was without the feathery edema of papilledema, elevation of the disks may have represented structural fullness. Retinopathy was not noted. Speech was dysarthric. Pleural effusion and slight cardiac enlarge-

Effect of anosmia on the appreciation of flavor.

A CENTURY AGO a controversy existed as to the role of the lingual nerve in the determination of tzste and flavor. In the past 100 years, however, considerable evidence has been collected supporting the assumption of Brillat-Savarinl and others that the flavor of substances is largely, if not altogether, dependent on olfaction.2.s Moncrieff4 has stated the opinion that “people suffering from loss of smell lose also what they call their ‘sense of taste,’ but which is really their odour component of the flavour.’’ Best and TayloI3 have said that blocking of the nasal passages by an upper respiratory infection seems to blunt the appreciation of taste, and it may then be impossible to distinguish between the taste of an apple and a pear, or a potato and a turnip. While observing that other factors may be of importance, such authors of physiology and psychology textbooks as Starling,6 Geldard,’ and Andrew@ have noted that the flavor of substances depends for the most part on olfaction. Little opposition to this assumption is noted in the pertinent literature. However, Hutchison,Q Crosland, Goodman and Hockett,”J and Leigh11 have reported cases of patients said to be suffering from anosmia who apparently continued to enjoy and recognize the flavor of various foods. In view of the difference of opinion revealed in the literature as to the importance of olfaction in the appreciation of flavor, the following report of a case may be of interest.

Treatment of Chronic Diabetes Insipidus

Polyuria and polydipsia of diabetes insipidus are usually treated by hormonal replacement.Posterior pituitary powder is the preparation of choice when it adequately controls the symptoms without side effects; when it does not, vasopressin tannate in oil should be used.Once the symptoms are controlled, the physician should determine whether the diabetes insipidus is secondary to involvement of the hypothalamic-neurohypophyseal system by a disease that will respond to operation, irradiation or medication

Pituitary insufficiency: a clue to the diagnosis of sellar tumors.

Pituitary insufficiency indicates disease in the region of the sella turcica and hypothalamus. Tumors of this region may cause pituitary insufficiency.A finding such as diabetes insipidus, or even amenorrhea, should alert the physician to the possibility of a pituitary tumor. Diagnosis may require such additional evidence as visual-field or x-ray changes.