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Epilepsia partialis continua following metrizamide cisternography.

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Furthermore, even ocular bobbing is not a sign of singular diagnostic importance [l]. The phenomenon of inverse
ocular bobbing (ocular dipping) is a unique newly recognized eye movement, but its diagnostic significance remains
uncertain at the present time.
Atypical Ocular Bobbing
Alan H . Ropper, M D
Knobler and his colleagues [ l ] reported in the February
Annals that intracerebral hematomas o r hyponatremia may
cause arrhythmic downward eye movements with slow
downward and fast upward components (inverse bobbing).
Their patients had status epilepticus prior to the appearance of these movements; in addition, one had documented
hypoxia. I believe that ocular dipping (or inverse bobbing)
movements frequently occur after hypoxic encephalopathy
121 and wonder if that was not the cause in the cases presented by Knobler e t al. O n the basis of two patients, one
autopsied and another with abnormalities o n C T scan, it
appears that diffuse cortical and perhaps bilateral basal
ganglia dysfunction causes the dipping movements [2].
In contrast to well-studied cases of bobbing in which lesions have been found in the rostra1 pons, there were no
brainstem abnormalities in the autopsied patient with ocular dipping 121. The diagnostic value and anatomical
significance of both ocular bobbing and dipping are diminished if dipping is considered a variant of bobbing. Like
roving eye movements which accompany it, dipping signifies a normal brainstem and a physiologically abnormal
cortex. The movements particularly suggest that hypoxia
has occurred and therefore may be helpful in the diagnosis
of coma. Instances of “atypical bobbing” that have been attributed to metabolic encephalopathy were incompletely
described, lacked supportive pathological changes, or were
more typical of dipping [3].
Department of Immunopathology
Scripps Clinic and Research Foundution
10666 N Tovrey Pines Rd
La Jolla, C A 92037
NeuroloKy-NeurosurgeryICU
Massachusetts General Hospital
Boston, M A 021 14
References
1. Knobler RL, Somasundaram M, Schutta HS: Inverse ocular
bobbing. Ann Neurol 9:194-197, 1981
2. Ropper AH: Ocular dipping in anoxic coma. Arch Neurol
38:297-299, 1981
3. Susac J, Hoyt W, Daroff R, Lawrence W: Clinical spectrum of
ocular bobbing. J Neurol Neurosurg Psychiatry 33:771-775,
1970
Reply
Robert L. Knobler, MD, PhD,
Mahendra Somasundaram, MD,
and Henry S. Schutta, M D
Both our cases and those described by D r Ropper 121 lend
themselves to the interpretation that inverse ocular bobbing (ocular dipping) is associated with diffuse cerebral
dysfunction. Hypoxia will probably prove to be an important cause for this finding. Inverse ocular bobbing has been
seen (H. S. S.) in two patients with hypoxia since publication of o u r report. However, the implication that this
finding is a sign that signifies intact brainstem function a
priori is unwarranted. The integrity of the brainstem
should be determined by appropriate testing of brainstem
function.
400
Annals of Neurology
Vol 10 No 4
October 1981
Refirences
1. Bosch EP, Kennedy SS, Aschenbrener CA: Ocular bobbing:
the myth of its localizing value. Neurology (Minneap) 25:
949-953, 1975
2. Ropper AH: Ocular dipping in anoxic coma. Arch Neurol
38:297-299, 1981
Epilepsia Partialis Continua
Following
Metrizamide
-.
.
Listernography
Zenji Shiozawa, MD,*t Hidenao Sasaki, MD,”
Yukio Ozaki, MD,” Takao Nakanishi, MD,”
and Yun Peng Huang, M D t
Bertoni et al [2] noted two patients with marked asterixis
following metrizamide myelography. W e recently observed
a patient who developed epilepsia partialis continua 131
following metrizamide cisternography.
A 32-year-olt!, right-handed man was admitted to the
hospital for evaluation of heaviness of the neck and dizziness. Past history was unremarkable; there was no record of
seizures, allergic disorders, o r drug abuse. Laboratory tests
were normal. Neurologically the patient was alert and his
mental function was normal. Segmental sensory dissociation was found on the face and in the neck ( C 4 ) .Deep tendon reflexes were decreased in the arms and increased in
the legs with occasional extensor responses. Muscle
strength was normal except in the tongue and neck. A
Romberg test showed unsteadiness. C T scans of the
craniospinal junction failed to disclose herniared tonsils.
Following premedication with anticonvulsants and
diazepam, cisternography was performed using 10 cc of
metrizamide (1,500 mg in total iodine concentration) via a
high lateral C 1-C2 puncture. Hypocycloidal tomography
was done with the patient in the left lateral recumbent position for sagittal cuts [ 4 ] .A type i Arnold-Chiari malformation [ I ] was diagnosed. During the procedure metrizamide passed over the cerebral hemispheres, mainly on
the left side, with relatively little dilution of its concentration.
Initially the patient tolerated the procedure well, but 4
hours after injection of metrizamide, epilepsia partialis
continua with repeated muscle twitchings appeared conjointly in the face and in distal portions of the right arm and
leg. The twitchings were mild at the onset, reached their
C T scans parallel t o the orbitomeatalplane 20 hours after
metl-izamide cisternography. Marked enhancement of the cortical gray and adjacent white matter of the left cerebral hemisphere, particularly i n the retrosylvian area, is obvious.
(Hounsjield unit 65.5 within the smallsquare on the left.)
peak at the fifth to eighth hour, and ended at the fifteenth
hour. Neurological examination revealed slight drowsiness,
motor aphasia, retrograde amnesia, and a mild degree of
weakness; there was hyperreflexia in the right upper and
lower extremities with a Babinski sign. All the findings
cleared after cessation of the seizures.
A noncontrast CT scan 20 hours after instillation of the
metrizamide disclosed diffuse enhancement o n the left side
of the brain, particularly posteriorly in the cortex and in the
adjacent white matter portions of the posterior frontal,
parietal, temporal, and occipital lobes (Figure). The findings suggest that transpial o r transcortical passage of metrizamide [ 5 ] had occurred. The delayed onset of symptoms correlated well with the circulation of metrizamide
over the cerebral convexity, suggesting that the peak concentration of contrast material coincided with the period of
maximum symptomatology.
*Institute of Clinical Medicine
The University of Tsukuba
I baraki 3 0 5 , Japan
+Division of Neuroradiology
The Mount Sinai School of Medicine
Fifth Ave and 100th St
New York, N Y 10029
References
1. Archer CR, Horenstein S, Sundaram M: The Arnold-Chiari
malformation presenting in adult life. A report of thirteen cases
and areview of the literature. J Chronic Dis 30:369-382, 1977
2. Bertoni JM, Schwartzman RJ, Van Horn G, Partin J: Asterixis
and encephalopathy following metrizamide myelography: investigations into possible mechanisms and review of the literature. Ann Neurol 9:366-370, 1981
3. Koshewnikow AJ: Eine besondere Form von corticaler Epilepsie. Neurol Centralbl 14:47-48, 1895
4. Roberson GH, Ellis G, Brismar J, Taveras JM: Cisternography
with metrizamide and hypocycloidal tomography. Acta Radio1
[Suppl] (Stockh) 3 5 5:3 14-322, 1977
5. Winkler SS, Sackett JF: Explanation of metrizamide brain
penetration: a review. J Comput Assist Tomogr 4:191-193,
1980
GABA Receptors
in Alcoholism
Ladislav Volicer, MD, P h D
The conclusion of the paper by Tran and co-workers [4]
suggesting that GABAergic mechanisms play a role in
chronic alcoholism is supported by a large body of evidence, but the exact mechanisms are less clear than
suggested by the paper’s discussion. Although animal experiments 13, 51 were quoted to support the finding of
increased y-aminobutyric acid (GABA) receptors in alcoholics, results of these experiments demonstrate the opposite. Ethanol-induced dependence in rodents results in a
diminished number of low-affinity G A B A receptors, while
withdrawal decreases the affinity of high-affinity receptors
[ 3 , 5 , 61. The difference between these data and changes of
GABA binding in alcoholics could be due to several factors. The patients were reported to have consumed beverages with a high alcohol concentration till the time of hospital admission, but the duration of their abstinence and the
presence or absence of withdrawal symptoms was nor
specified. In animal experiments, GABA binding was determined either soon after the last ethanol administration
Letters 401
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metrizamide, partiality, following, epilepsies, cisternographic, continue
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