Abcess of the brain / by Heinrich Neumann.

  • Neumann, Heinrich.
Date:
[1930?]
Catalogue details

Licence: In copyright

Credit: Abcess of the brain / by Heinrich Neumann. Source: Wellcome Collection.

    11/18 page 51
    The post-operative course was this time rather stormy : the child was very drowsy for several days, and suffered from severe headaches and frequent vomiting. However, he was sufficiently recovered to leave hospital on August 1, 1929, one month after operation. Headache recurred during the first two weeks in August, but then disappeared. The first indication of any failure of vision occurred on August 21, when the mother noticed that the boy tripped over curb-stones. In September he began to fall over objects and to feel his way about as he walked. Ophthalmological examination was carried out on October 14, apparently for the first time. The boy could not count fingers. The discs showed severe papilloedema and optic atrophy, and there was exudate around each macular region. Two teeth were removed on October 15. Condition on examination, October 29, 1929 : Left eye completely blind ; right eye per¬ ception of light only. No reaction of left pupil to direct light, moderate reactionmf right pupil. Severe secondary optic atrophy, with 2 • 5 D. swelling on right side, but no swelling on left side. Exudate around each macula. No other physical signs except generalized hypotonia and diminished tendon-jerks, and slight enlargement of the head. The boy was cheerful and, apart from his blindness, free from symptoms. Lumbar puncture : pressure 230 mm. In unilateral Queckenstedt tests, the usual rise of pressure occurred when the right jugular vein was compressed, but there was no rise of pressure when the left jugular vein was compressed. In this case a thrombosis of the left lateral sinus had thus evidently developed since the lateral sinus was opened at the second operation on the left mastoid process. The cerebro¬ spinal fluid was clear. It contained one cell per c.mm. ; 0-02% protein. Cultures sterile. Comment.—As far as it is possible to judge from the available evidence, this appears to be a case of the so-called arachnoiditis or serous meningitis. The pathology of “ arachnoiditis ” is at present quite obscure. In the only case of the condition in which I have been able to make a histological examination, the arach- noidea showed no evidence of inflammation, and I think the term “ arachnoiditis ” is probably an incorrect one. All that we know about the pathology of the condition is that there is hydrocephalus, but whether this is due to increased formation of cerebrospinal fluid, or to decreased absorption of cerebrospinal fluid, or to a combina¬ tion of both these factors, is at present unknown. The condition follows middle-ear and mastoid infection, but it may also occur without any demonstrable focus of infection, either in the ears or elsewhere. This is the first case of arachnoiditis that I have seen in which thrombosis of the lateral sinus has been demonstrated. Such an occurrence would tend to interfere with the absorption of cerebrospinal fluid, and thus to aggravate the rise of intra¬ cranial pressure. This may account for the extreme degree of destruction of the optic discs by papilloedema and atrophy. The case is typical in the absence of severe headaches, except for a short period at the beginning of the illness. This absence of headache is not to be explained solely by the fact that in this instance the patient was a child whose head could expand in response to increased intracranial pressure, for absence of severe headache is a noticeable feature also in adults. The condition tends to recover spontaneously. I have seen two cases—both in children—in which perfect recovery occurred without any treatment at all. In one of these the papilloedema reached 4 diopters before it began to subside; in the other the swelling was never higher than 2 diopters. In both cases vision eventually became normal. In other cases, however, although all the symptoms clear up, they do not do so until vision is seriously affected. The little boy whose case I have just described is now permanently blind, though perfectly well in other ways. From my experiences with this condition I believe that a cerebellar decompression, performed before the destruction of the optic discs has become far advanced, is a sure method of preserving vision. It should be carried out in every case in which the papilloedema becomes at all severe, or in which there is any sign of lowering of visual acuity. In one case of this condition in which the patient was practically blind, vision returned in a most dramatic manner after a cerebellar decompression had been done. The operation, however, cannot be expected to effect a return of vision after blindness has been present for some weeks. Nevertheless, I would have been prepared to operate
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