When Dr. Stevens asked me to write a paper for the Bureau of Obstetrics and Pediatrics I very blithely promised to discuss meningismus and give a report of a case. Since then, however, I have had ample time in which to regret my choice of subject matter. I have a case of meningismus, to be sure, the report of which will be given shortly, but to find enough data about meningismus to be incorporated into a discussion would seem to be an almost Herculean task.
Of course the difficulty lies in the fact that meningismus is seldom, nowadays, considered as a clinical entity, a disease sui generis. In two textbooks on pediatrics, published within the last ten years and in Blumers Bedside Diagnosis, the condition is considered as occurring chiefly in children as an accompaniment of any acute, infectious disease. Fishers Diseases of Children, edition of 1896, does not mention meningismus by name but discusses it under the title of Acute Simple Meningitis. Ten years later Raues Diseases of Children deals with meningismus in the same manner.
I do not hold with the earlier authors that meningismus is a simple acute inflammation of the meninges, though I do agree that meningitis may occur in the course of some other acute infection. No do I agree with the implication suggested by later writers that meningismus must occur as a complication of some other acute disease. I believe that the case to be reported later will show that this condition does present itself as a separate clinical entity and that it is not an infection, but an irritation of the meninges, probably of toxic origin.
I am quite ready to admit, however, that most cases of meningismus are met in conjunction with other acute diseases. Observation during more than ten years of general practice has led me to the conclusion that meningismus, occurring as a disease sui generis, is extremely rare and that almost without exception it is a condition of childhood.
Since meningismus most commonly appears at the onset of, or during the course of, an acute illness, it should be quite in order at this point to list those conditions which are most apt to give rise to this syndrome. In infants and young often in connection with acute gastrointestinal disturbances. In older children the condition is not infrequently seen during pneumonia. In otitis media and mastoiditis meningismus may appear. Teething may rarely give rise to it. In brief, any condition associated with high temperature and the production of toxic substances can present the manifestations of meningismus.
The symptoms of meningismus are those which are wont to be associated with the various acute meningismus. These are so familiar that it should be unnecessary for them to be discussed in detail. Suffice it to say that any or all the symptoms of true meningitis may be present in meningismus, though in general there are less apt to be focal symptoms in the latter.
Of course, when evidence of cerebral involvement appears, in a case under our care we want to know whether we have to deal with meningismus or with a more serious condition. The chief conditions to be differentiated are: acute anterior poliomyelitis, pneumococcic meningitis, meningitis due to the pyogenic organisms, influenzal meningitis, and meningococcal meningitis. The differential diagnosis can be dismissed in short order-I am against lengthy discussion of perfectly obvious facts- by stating that the lumbar puncture is the method by which the true condition can be determined.
In meningismus the spinal fluid is perfectly normal and no organisms can be cultured from it. In the other diseases the spinal fluid presents typical pictures and, in addition, the causative organism can usually be found by culturing. Lumbar puncture is a procedure easily carried out in the home with a little intelligent co-operation from members of the family, so that no physician needs to remain long in doubt as to the diagnosis when cerebral symptoms appear in any of his cases.
And now for the presentation of the case, which I hope you are all eagerly awaiting:.
The patient was a boy of six years of age. On August 13, 1936 he went to the circus. When he returned to his home in the evening he complained of headache and nausea and would eat no supper. I saw the child the same evening about 8: 30, in the course of a visits to his mother. I examined him very casually and, as casually, prescribed a dose of Belladonna 200. I saw the patient again the next morning. His temperature was 104 by rectum. He had a very flushed face, a hot, dry skin and the pupils were widely dilated.
He complained solely of nausea. I again gave a dose of Belladonna 200. On the 15th I called again to see this little patient and found conditions very much worse. The temperature had risen to 105.4 by rectum. The pulse and respiration were both very rapid. There was twitching of all the muscles of the face. The hands trembled. The limbs jerked. He was delirious. The pupils were dilated but reacted normally. The patella reflex was hyperactive. There was a positive Kernig. The neck was rigid. He complained of frontal headache and of pain in the neck. It was evident to me that Belladonna was not the remedy.
There were some symptoms of Gelsemium present so that drug was given, a single dose of the 200. On the 16th when I made my morning visit there seemed to be a slight improvement. The temperature had dropped to 103.8 by rectum. there was less twitching of the face and jerking of the limbs. Kernigs sign was negative. However, at 2 oclock that afternoon the boy had an attack of furious delirium in which he jumped from his bed in a rage, striking and biting at his nurse. This attack so exhausted him that when I arrived in a hurry, he was quiet in bed. But the neurological signs were again positive. I decided then to hospitalize the child for observation.
The first procedure at the hospital was to perform a lumbar puncture. The spinal fluid appeared under very slightly increased pressure and was perfectly clear. An analysis showed the pressure of a trace of globulin and the reduction of sugar. A cell count showed nine cells per c.c., quite within normal range.
A red, white and differential blood cell count was next done. The erythrocytes were 4,568,000 the leucocytes were 20,350 of which 88 percent were polymorphonuclears and 12 percent lymphocytes. The hemoglobin was 78 percent.
Examination of the urine showed a cloudy, straw-colored specimen, acid in reaction, having a specific gravity of 1.018. There was trace of albumin, no sugar, a high trace of acetone and a positive diacetic acid reaction. Under the microscope the sediment showed an occasional course granular cast, a rare red blood cell, and an occasional pus cell.
On admission to the hospital this boys temperature was 105.4. The pulse was 152 and the respirations 40. Physical examination revealed no other findings than the neurological signs already enumerated.
In view of the fact that no definite pathological process had been demonstrated by laboratory procedures, and because a closer study of the symptomatology had indicated Aconite as the needed therapeutic agent, I elected to give this remedy without further delay. One powder of the 30th was dissolved in 10 drams of water and the nurse was instructed to give one dram of the solution every three hours for three doses.
The first dose was given at 5 p.m. The second dose was given at 8 p.m. by which time the temperature had dropped to 103.4 and the patient had broken out into a profuse perspiration. At midnight, when the third dose was given, the temperature had subsided to 100.4 by mouth (approximately 101.4 rectally). I knew then that we had the thing licked. At 4 a.m. on the 17th the temperature was 99.1 per os and twelve hours later it was normal. From this time on the recovery was uneventful. There was a slight elevation of the temperature on the 20th which was due to constipation and which was adequately controlled by a saline enema.
For the sake of the record a white blood cell count was made on the 19th which showed 10,325 leucocytes of which 52 percent were polymorphonuclears and 48 percent were lymphocytes, normal findings in a lad of six years. Urinanalysis on the same day was normal.
An interesting sequelae to this boys experience was the complete change of personality. Where previously he had been rather dull and stupid, preferring to stay by himself than to take part in the play of other children, he now became a normal, happy child ready for any sort of fun or mischief.
Allan D. Sutherland was born in Northfield, Vermont in 1897, delivered by the local homeopathic physician. The son of a Canadian Episcopalian minister, his father had arrived there to lead the local parish five years earlier and met his mother, who was the daughter of the president of the University of Norwich. Four years after Allan’s birth, ministerial work lead the family first to North Carolina and then to Connecticut a few years afterward.
Starting in 1920, Sutherland began his premedical studies and a year later, he began his medical education at Hahnemann Medical School in Philadelphia.
Sutherland graduated in 1925 and went on to intern at both Children’s Homeopathic Hospital and St. Luke’s Homeopathic Hospital. He then was appointed the chief resident at Children’s. With the conclusion of his residency and 2 years of clinical experience under his belt, Sutherland opened his own practice in Philadelphia while retaining a position at Children’s in the Obstetrics and Gynecology Department.
In 1928, Sutherland decided to set up practice in Brattleboro.