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46
It is probable that the position of a cerebral tumour or abscess may affect
the characters of the fluid. If superficial and involving the cortex, thereby causing
pressure on the cerebral or meningeal vessels, the growth is likely to cause escape
of blood plasma or even blood cells into the meninges, and so an increase in the
amount of intra-cranial fluid as well as of its protein content, with little alteration
in the total number of cells. When, however, the tumour is deep-seated, not
exercising pressure on the superficial membranes, nor involving the lateral ventricles,
there is less likelihood of change in composition of the fluid. Very seldom are cells
derived from the neoplasm to be recognised as such in the centrifugation deposit.
Vascular Lesions due to changes affecting the cerebral vessels and blood supply.—
Included in this category were four cases of paralysis, in which the provisional
diagnosis was respectively uraemia, meningitis or cerebral irritation and encephalitis
lethargica. The fluid showed little departure from the normal, except slight increase
in the protein content and traces of blood in two cases without yellow discolouration
of the supernatant fluid after centrifugation of the blood cell deposit. Traces of
blood may or may not occur in cases of recent haemorrhage with yellow discolouration
or xanthochromia of the cerebro-spinal fluid, but the latter condition when present
is more indicative of old haemorrhage or compression of the cord by tumour. Uraemia
was contra-indicated by the fact that urea was not found in more than the normal
trace (.04 per cent.)
It was, therefore, possible to exclude the suggested diagnoses, with the exception
of encephalitis, which as already mentioned has so often to be taken into consideration
in the differentiation of other forms of cerebral disease and is well known as a cause
of hemiplegia.
From the subsequent course of each of the four cases they were ultimately
diagnosed as follows:—
(1) Puerperal hemiplegia (Moxon's)—probably due to arterial thrombosis,
in a woman aged 38, accompanied by epileptiform fits at the onset, with later
paralysis of the right arm and leg. Subsequently the patient was discharged
after 3 months, relieved.
(2) Cerebral haemorrhage due to the toxaemia of pregnancy in a woman
aged 17, marked by convulsive attacks affecting the left side and proving fatal
6 weeks after the onset.
(3) Recurrent haemorrhages into the internal capsule in a man aet. 61,
due to cerebral arteriosclerosis, proving suddenly fatal from a fresh haemorrhage.
(4) Cerebral softening of the basal ganglia due to arterial thrombosis,
which proved fatal in less than a fortnight after the onset in a woman aged 47.
Circulatory disturbance whether due to chronic inflammatory changes (usually
syphilitic endarteritis) or to degenerative thickening of the arteries (cerebral arteriosclerosis)
may give rise not only to cerebral haemorrhage and thrombosis with
softening, but also to changes in the mental state of a patient without the occurrence
of paralytic symptoms.
In two examples of paralysis due to cerebral haemorrhage followed by dementia,
as well as in a case of simple dementia without paralysis attributable to cerebral
arteriosclerosis, the cerebrospinal fluid showed little change from the normal, but
the negative results of the Wassermann and colloidal-benzoin reactions contraindicated
syphilis as a cause. This indeed is the extent of the information which
the cerebrospinal fluid can be relied upon to yield in such cases of simple cerebral
arteriosclerosis uncomplicated by syphilitic endarteritis. Moreover, the forms of
mental confusion and changes in character attributable to either of these conditions
may in certain cases be difficult to distinguish from similar states occurring as the
result of encephalitis, nor will the cerebrospinal fluid provide a clue except evidence
for or against syphilis by means of the special reaction tests.