Neurosyphilis : $b Modern systematic diagnosis and treatment presented in one hundred and thirty-seven case historiesSouthard, Elmer Ernest
Science
Neurosyphilis : $b Modern systematic diagnosis and treatment presented in one hundred and thirty-seven case histories
Southard, Elmer Ernest
Neurosyphilis
=TABETIC NEUROSYPHILIS (“tabes dorsalis”) with symptoms of cerebral
origin producing a picture resembling taboparetic neurosyphilis
(“taboparesis”). Autopsy.=
=Case 43.= Robert Allen was the fifth case of error in the diagnosis of
general paresis analyzed some years since from the staff meeting records
of the Danvers Hospital. The Allen case resembles the case of Elizabeth
Brown in that there was a combination of tabetic phenomena with cerebral
lesions of a non-paretic character at autopsy. But although there seemed
to be an utter absence of inflammatory cells (lymphocytosis) in the case
of Elizabeth Brown (42), there were some slight perivascular cell
accumulations in the Allen case, with a few mononuclear cells suggestive
of lymphocytes. The cerebrum, however, failed to show plasmocytosis. It
was seriously diseased, showing a marked neuroglia proliferation about
the atrophic nerve cells.
Robert Allen was a printer coming from a long-lived race. The following
are the main facts:
Married in 1875 (two children, healthy); again married in 1893 (one
child, healthy). Compositor from 1890. In 1898 and 1899 girdle and
lancinating pains. Thereafter for several years gait was unsteady.
During 1904 and 1905 freedom from pains and improvement in gait but
gradually increasing irritability and nervousness. Stopped work on last
of March, 1905, owing to sudden increase of irritability, emotionality,
boastfulness, expansive schemes, and ataxia.
Habits: no tobacco, very little alcohol at long intervals. No drug
habits, no sexual irregularity known.
Committed to Danvers April 3, 1905, with slight muscular development,
poor nutrition, acne, irregular, poorly preserved teeth, gingivitis,
flat-foot, slight radial arteriosclerosis, slight arcus senilis, a few
hyaline casts, leucocytes, epithelial cells, and trace of albumin in the
urine, scar in sulcus, and enlarged inguinal lymph nodes.
Ataxic gait, Romberg’s sign, fibrillary twitching of chest, abdominal
and facial muscles when standing; right pupil slightly larger than left,
pupillary margins irregular, light reactions (electric bulb test) both
consensual and direct absent, slight pupillary reaction in
accommodation; biceps, triceps and wrist reflexes lively and equal;
abdominal, cremasteric and plantar reflexes normal, knee-jerks, Achilles
and front taps negative even on reinforcement.
The patient himself stated that his ataxia began in 1904, that he had
been under treatment for swelling of legs and feet and pain in limbs
since 1903, and that there had been some trouble with limbs since 1895.
He had been told that his disease was lead-poisoning. About three weeks
before commitment patient said he had had an attack of unconsciousness.
Public-domain text, read in full here on John Shaqi.
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