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Effect of carbamazepine on blood elements.

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became more prominent. These changes persisted for approximately fifteen minutes before resolving. An intravenous injection of normal saline had no effect.
A reciprocal antagonistic relationship between dopamine
and acetylcholine neurotransmission in the basal ganglia
has been discussed widely. W e have found that physostigmine often worsens Parkinson disease and other extrapyramidal disorders characterized by bradykinesia, rigidity,
and tremor. This effect is sometimes useful in the identification of early and relatively mild parkinsonian syndromes. In our experience, intravenous physostigmine and
benztropine produce only minor and inconsistent effects in
choreatic disorders [ 1, 21. Patients with generalized or focal
dystonias have been similarly unresponsive. T h e adverse
effect of physostigmine in our patient with Wilson disease
suggests that striatal dopamine deficiency may play a role in
producing his symptoms. Although cerebrospinal fluid
homovanillic acid following oral probenicid loading was
greatly reduced (less than 10 ng per milliliter), the patient
has failed to improve after treatment with L-dopa. Treatment with D-penicillamine has recently begun.
Supported by Veterans Administration research funds.
References
1 . Tarsy D, Bralower M: Deanol acetamidobenzoate treatment in
choreiforrn movement disorders. Arch Neurol 34:756-758,
1977
2. Tarsy D, Leopold N , Sax DS: Physostigmine in choreiform
movement disorders. Neurology (Minneap) 24:28-33, 1974
Effect of Carbamazepine
on Blood Elements
Joel Y . Rutman, M D
Since carbamazepine (Tegretol) has been approved for use
in the United States for the treatment of epilepsy, it has been
found to be an effective anticonvulsant for grand ma1 and
psychomotor seizures. Despite the warning in Physicians’
Desk Reference of “serious and sometimes fatal abnormalities of blood cells,” the drug has been used with increasing frequency, and there has been less apparent need for
periodic checking of the blood elements than would have
originally been supposed. A recent report from LOS Angeles found no significant abnormalities of the blood in a
series of 6 1 children treated from one to five years with
carbamazepine [I].
platelet tests were normal prior to initiation of the drug.
Two weeks later she developed generalized petechiae. The
hemoglobin and hematocrit were normal, as was the differential count. The white blood cell count was 4,000 per
cubic millimeter and there were 11,000 platelets. Liver
chemistry values were normal. Carbamazepine was discontinued. A repeat platelet count two days later was 38,000;
four days later it was 184,000. The petechiae disappeared,
and the girl has had no further hematological problems.
The necessity for periodic evaluation of the blood elements in patients taking carbamazepine is reemphasized.
Reference
1. Huff R, Schain RJ: Long-term experiences with carbarnazepine
(Tegretol) in children with seizures. Presented at the 6th Annual
Meeting of the Child Neurology Society, Charlottesville, VA,
Oct 6, 1977
Ophthalmoscopy in
Examination of Patients
with Vestibular Disorders
David S. Zee, M D
In the differential diagnosis of vestibular disorders, it is
helpful to know if apatient with nystagmus can diminish the
velocity of the slow phase by fixation. If the patient can, the
lesion causing the nystagmus is usually located within the
peripheral vestibular apparatus. If the velocity of the slow
phase of nystagmus is unchanged or increased by fixation,
the lesion is usually located within central vestibular connections [ 13. Normally, electronystagmography must be used to
determine the effect of fixation on the velocity of the slow
phase of nystagmus. However, a qualitative determination
can easily be made at the bedside with an ophthalmoscope.
Method
We examined a 16-year-old girl and placed her on carbamazepine, 200 mg orally three times a day, following
inadequate seizure control with Dilantin and Mysoline.
White blood cell count and differential, hemoglobin, and
During ocular examination in a dimly lit room, the patient
is instructed to fixate on a distant target with one eye while
the examiner observes the movement of the optic nerve
head of the other eye with the ophthalmoscope. (The optic
disc islocated behind the axis of rotation of the globe, so the
disc and the visual axis rotate in opposite directions.) The
patient’s fixating eye is then covered, and the rate of drift of
the optic nerve head (which corresponds to slow phase
velocity) is compared to that observed during fixation. If
fixation suppression of nystagmus is intact, the optic nerve
head either begins to drift or drifts more rapidly when the
fixating eye is covered. T h e patient’s e y e is then uncovered
and the rate of drift is again assessed. T h e fixating eye can be
covered and uncovered several times to confirm a change in
the velocity of the slow phase.
This test is most reliable if the drift rate does change when
From the Department of Pediatrics, University of Texas Medical
School, San Antonio, T X 78205.
From the Departments of Neurology and Ophthalmology, The
Johns Hopkins Hospital, Baltimore, M D 21205.
Letters
373
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