drochloride (Prolixin) and the thioxanthene thiothixene (Navane) follow
haloperidol in potency.
The low-potency neuroleptic agents,
including the aliphatic phenothiazine
chlorpromazine (Thorazine) and the
piperidine phenothiazine thioridazine
(Mellaril), while associated with oculogyric crises, are much less likely to
cause an oculogyric crisis. This can
most likely be attributed to the inherent anticholinergic effect of these

agents.2,3

Abraham Dorevitch, PharmD
Talbia Psychiatric Hospital
PO Box 39
Jerusalem, Israel

1. Clough CG, Plaitakis A, Yahr MD: Oculogyric crises and parkinsonism: A case of recent
onset. Arch Neurol 1983;40:36-37.
2. Kessler KA, Waletsky JP: Clinical use of the
antipsychotics. Am J Psychiatry 1981;138:202\x=req-\

208.
3. Johnston JA, Coleman JH, Callaway JT, et
al: Protocols for the use of psychoactive drugs:
Part I. Protocol for the treatment of psychosis
with antipsychotics. J Clin Psychiatry 1980;
41:375-377.

cal and cardiac examination results were
not remarkable. There was right-sided
hemiparesis; strength was reduced to four
fifths in the extensor muscles of the upper
extremity and to three fifths in those of
the lower extremity. There was a right
plantar reflex to the extensor muscle, as
well as mild ataxia in the right arm and
severe ataxia in the right leg. The patient
could not stand up without assistance. Sensation was normal. No visual field defects
could be observed, and there was no speech
disturbance. The patient had binaural per¬
ception deafness. The other cranial nerves,
including those for ocular and facial motility function, were normal. There were no
carotid bruits. The ECG and results of
blood chemistry tests and CSF analysis
were normal. An EEG showed a back¬
ground rhythm of 8 to 9 Hz, sometimes
slowing to 7 to 8 Hz; infrequent theta
waves were recorded in the temporal leads.
Brain-stem auditory evoked responses
were not obtainable bilaterally due to
hearing loss. A contrast-enhanced CT scan
two weeks after onset showed a hypodense
area (density, 17 hyperemia units; 10 mm
in diameter) in the basis pontis on the left
(Figure). Four weeks later, muscle
strength was normal, but ataxia was still

present.
Pontine Ataxic Hemiparesis

To the Editor.\p=m-\Ina recent article,
Ichikawa et al (Archives 1982;39:585\x=req-\
586) discussed the possible causes of
ataxic hemiparesis. We report a case
of ataxic hemiparesis with an ischemic lesion in the basis pontis, clearly
shown by computed tomography

(CT).

Report of a Case.\p=m-\A72-year-old man
experienced weakness of the right arm and
right leg on awakening and noticed some
numbness of the right hand. On admission
to the hospital two days later, his BP was
slightly elevated (160/100 mm Hg). Physi-

Comment.—Ataxic hemiparesis is
caused by different types of lesions,
localized in the basis pontis, midbrain,
or internal capsule and verified by CT
scan or autopsy. Ischemie,1 hemorrhagic,2 or metaplastic3 lesions in the
basis pontis and a midbrain mass4
have been described. Reports of lacunar infarcts in the internal capsule,
shown by CT scan, are now abun¬
dant.512 To our knowledge, this is the
first case of CT-visualized pontine
lacunar infarction in a patient with
"typical" ataxic hemiparesis, as
described by Fisher.1 Sakai et al13

reported an atypical case of ataxic
hemiparesis with trigeminal weak¬
ness, caused by a lacunar lesion in the
basis pontis and confirmed by a CT
E. Van Buggenhout, MD
I. Dehaene, MD
M. Van Zandijcke, MD
Department of Neurology
AZ St Jan
B-8000 Brugge

Belgium

1. Fisher CM: Ataxic hemiparesis: A pathologic study. Arch Neurol 1978;35:126-128.
2. Schnapper RA: Pontine hemorrhage presonting as ataxic hemiparesis. Stroke 1982;13:518\x=req-\
519.
3. Radhakrishnan K, Malhotra AK, Shridharan R, et al: Ataxic hemiparesis: Clinical, electro-$
physiologic, radiologic and pathologic observations. Clin Neurol Neurosurg 1982;84:91-100.
4. Bendheim PE, Berg BO: Ataxic hemiparesis
from a midbrain mass. Ann Neurol 1981;9:405\x=req-\
407.
5. De Renzi E, Nichelli P, Crisi G: Hemiataxia
and crural hemiparesis following capsular
infarct. J Neurol Neurosurg Psychiatry 1983;
46:561-563.
6. Donnan GA, Tress BM, Bladin PF: A prospective study of lacunar infarction using com-

puterized tomography. Neurology 1982;32:49-56.
7. Iragui VJ, McCutchen CB: Capsular ataxic
hemiparesis. Arch Neurol 1982;39:528-529.
8. Jokelainen M, Pilke A: Ataxic hemiparesis.
Arch Neurol 1983;40:326.
9. Perman GP, Racy A: Homolateral ataxia
and crural paresis: Case report. Neurology 1980;

30:1013-1015.
10. Rougemont D, Baron JC, Lebrun-Grandie
P, et al: D\l=e'\bitsanguin c\l=e'\r\l=e'\bralet extraction
d'oxyg\l=e`\nedans les h\l=e'\mipl\l=e'\gieslacunaires: Etude
s\l=e'\mi-quantitativepar l'oxyg\l=e`\ne-15et la tomographie d'\l=e'\mission.Pathol Biol 1982;30:295-302.
11. Tredici G, Bogliun G, Sanguineti I: Capsular ataxic hemiparesis. Arch Neurol 1983;40:326.
12. Weisberg LA: Lacunar infarcts: Clinical
and computed tomographic correlations. Arch
Neurol 1982;39:37-40.
13. Sakai T, Murakami S, Ito K: Ataxic hemiparesis with trigeminal weakness. Neurology

1981;31:635-636.

Left, Contrast-enhanced computed tomographic scan two weeks after
onset of right-sided ataxic hemiparesis. Right, Hypodense area in left pons.

Downloaded From: http://archneur.jamanetwork.com/ by a University of Edinburgh Library User on 06/20/2015