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"This is probably the most discussed symptom or sign in connection with meningitis of recent
times. Kernig, a physician of St. Petersburg, first described it in 1882, and published his results in
1884. He observed it in various forms of meningitis and confirmed the diagnosis at autopsy. The sign
consists in an inability to extend the leg fully when the thigh is placed at right angles to the trunk.
Kernig observed this sign when he attempted to set the patient at the edge of the bed and straighten
the legs. He noticed that this was impossible, and following up his observation he found that this
was the case in all forms of meningitis. Osier simplified the sign very much by showing that it may
be elicited with the patient in the recumbent posture by placing the thigh at right angles to the trunk
and then attempting to extend the leg on the thigh. Kernig not only found this sign in meningitis
and considered it pathognomonic, but he observed it in the convalescence from the disease when
the patient was up and walking about.
These observations have been confirmed with reservations. Kernig's sign is not pathognomonic
of meningitis any more than rigidity of the neck. It is, however, very valuable and completes the
picture of the disease. It is present in diseases of the most diverse nature where cerebral symptoms
are present and toxaemia is great. The writer has seen it repeatedly in pneumonia with meningism
in children, and it has been observed in adults in some diseases, such as typhoid fever.
It is important to recognize what is and what is not the Kernig's sign, especially in meningitis.
In some cases an attempt to straighten the leg on the thigh will be resisted at an angle of 135° and in
others at an angle of 90°. It is therefore but fair to Kernig to include his sign between these
two variations. Unfortunately this sign may be absent in malignant forms of cerebrospinal
meningitis, especially in those with collapse symptoms, in which the patient a day or two after the
onset is seized with a chill and goes into a condition of complete collapse, due, perhaps, to increase of
fluid in the ventricles. In these patients the Kernig sign may be absent, although it may reappear
on a subsequent day. It may be absent at the onset of an ordinary attack and appear after the disease
has lasted a day or two. It is present in the majority of cases at some time in the course. As has
been intimated, it may not be present at critical periods. ... As has been intimated, the Kernig sign
is present in other forms of meningitis, but in tuberculous meningitis, especially in children, its presence
is not so constant and in the cases studied by the writer it was absent in fully one-third. It is not to
be relied on in very young infants in whom there is a muscular tonicity of both upper and lower
extremities which is normal and becomes exaggerated on the onset of the least illness. Its occurrence
in children below two years of age is variable for reasons which the writer cannot explain."
In the light of the foregoing, Kernig's sign loses value as a pathognomonic sign even of meningitis ;
but further observations as to its occurrence in diseases other than meningitis seem much to be needed.
The net result of taking the clinical evidence by itself in many cases of suspected cerebro-spinal
fever is to leave the physician frankly baffled in his attempt to make an exact diagnosis. He finds
that the ascertained signs and symptoms may be caused by, and point to a variety of diseases. He
can get no further evidence, as he would in other diseases, by noting pathological changes during
life. He cannot watch or feel or auscultate the working of the disordered organ. "Physical signs"
are almost non-existent, and the result is that in few diseases does he find himself so baffled and so
little able to make a diagnosis on clinical signs alone.
Of the post-mortem findings it may be said that in meningitis the evidence gained by actual
inspection and examination of the diseased organs does not differ in value from that similarly
obtained in other diseases—in a word, post-mortem evidence is the most trustworthy of all, but in
this connection it has the limitation, that by a mere post-mortem examination it may not be possible to
differentiate cerebrospinal fever from other forms of meningitis.
Bacteriology comes in, however, and offers to clear up the whole case. It claims to clinch the
diagnosis beyond all shadow of doubt. Little wonder then that implicit reliance comes to be placed
on the bacteriological finding ; and that makes it all the more necessary to examine closely the
value of this class of evidence.
The causal micro-organism has been thus described :—
"In 1887 Weichselbaum described an organism, the Diplococcus intracellular is meningitidis,
which was probably the same as one previously found by Leichtenstern. In the tissues the organism
is almost constantly within the polynuclear leucocytes. In cultures it has well characterized
features, and is distinguishable from the pneumococcus. Since Weichselbaum's observations this
organism has been met with in all carefully studied epidemics of the disease. In the Boston
outbreak, in 35 of the cases on which post-mortem examinations were made, the diplococci
were demonstrated in all but 4, in one of which they had previously been found in fluid
withdrawn by spinal puncture. The other 3 cases were chronic. The recent studies, too,
in Paris and Germany and in the United States have all been confirmatory of the constant
association of this organism with the disease." (Osier, Principles and Practice of Medicine,
Ed. 1905, p. 159.)
Here at last we seem to be on safe ground. Once the meningococcus—as the organism is commonly
called—is recovered, all uncertainty is at an end. If it is present, the disease is cerebrospinal
fever, and it is not that disease, if the meningococcus is not recoverable. And so it comes about
that the meningococcus is held to be at once the hall mark and the cause of the disease—which, indeed,
is termed meningococcal meningitis. This would be very simple if it were the whole story, but is
the meningococcus found exclusively in this disease ? Is it never found in any other class of case ?
The value of the meningococcus as a pathognomonic sign clearly turns upon these questions—some
answer to which is given below.
Here then are the three groups of evidence—the clinical, unreliable when taken alone; the