References
1. Asburv AK: Proximal diabetic neuroDathv. Ann Neurol
~~

~I

I

2:1791180, 1977
2. Blom S: EMG analysis of the lumbar musculature in patients
operated on for lumbar disc disease. J Newosurg 26:25-30,
1967
3. Chokroverty S, Reyes MG, Rubino FA, Tonaki H: The syndrome of diabetic amyotrophy. Ann Neurol2:181-194,1977
4. Compere E L The symptom-complex of visceral-spinal pain.
I11 Med J 74:434-442, 1938
5. Donovan WH, Sumi SM: Diabetic amyotrophy: a more diffuse process than clinically suspected (abstract). Arch Phys
Med Rehabil 55:568, 1974
6. Ellenberg M: Diabetic neuropathy: clinical aspects. Metabolism 25:1627-1655, 1976
7. Garland H: Diabetic amyotrophy. Br Med J 2:1287-1290,
1955
8. Isaacs H, Gilchrist G: Diabetic amyotrophy. S Afr Med J
34:501-505, 1960
9. Kellgren JH: On the distribution of pain arising from deep
somatic structures with charts of segmental pain areas. Clin Sci
4:35-46, 1939
10. LeBan MM, Grant AE: Occult spinal metastases-early EMG
manifestations. Arch Phys Med Rehabil 52:223-226, 197 1
11. Lewis T, Kellgren JH: Observations relating to referred pain,
visceromotor reflexes and other associated phenomena. Clin
S C4147-71,
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1939
12. Locke S, Lawrence DG, Legg MA: Diabetic amyotrophy. Am
J Med 34:775-785, 1963
13. Longstreth GF, Newcomer AD: Abdominal pain caused by
diabetic radiculopathy. Ann Intern Med 86: 166-168, 1977
14. Mulder DW, Lambert EH, Bastron JA, Sprague RG: The
neuropathies associated with diabetes mellitus. A clinical and
electromyographic study of 103 unselected diabetic patients.
Neurology (Minneap) 11:275-284, 1961
15. Raff MC, Sangalang V, Asbury AK Ischemic mononeuropathy with diabetes mellitus. Arch Neurol 18:487-499,
1968
16. Schulz A: Diabetlsche Radiculopathie der unteren Thorakalsegmente mit Bauchdeckenparesen. Verh Dtsch Ges Inn
Med 72:1171-1175, 1966
17. Schulz A: Brennende Schmerzen an Rumpf und Oberschenkel mit Bauchdeckenparesen. Dtsch Med Wochenschr 97:
1568-1569, 1972
18. Seitz D: Zur Klinik und Pathogenese der Polyneuritis diabetica. Dtsch 2 Nervenheilkd 175:15-37, 1956
19. Spritz N: Nerve disease in diabetes mellitus. Med Clin North
Am 62:787-798, 1978
20. Streib E, Daube J R Electromyography of paraspinal muscles
(abstract). Neurology (Minneap) 25:386, 1975
21. Streib E, Wilbourn AJ, Mitsumoto H: Spontaneous electrical
muscle fiber activity in polymyositis and dermatomyositis.
Muscle Nerve 2:14-18, 1979
22. Subramony SH, Wilbourn AJ: The varied spectrum of diabetic amyotrophy; EMG features (abstract). Electroencephalogr Clin Neurophysiol 45:2 1P-22P, 1978
23. Treanor WJ: Diabetic polyradiculopathy:a syndrome in need
of definition (abstract). Arch Phys Med Rehabil 55:592-593,
1974
24. Wessely P, Schnaberth G: Kasuistischer Beitrag zu einer
seltenen Lokalisation diabetischer Neuropathie. Wien Klin
Wochenschr 85:710-712, 1973

“Wrong-Way Eyes’’ in
Supratento rial Hemorrhage
Michael S. Pessin, MD,* Lester S. Adelman, M D , t
Robert J. Prager, MDJ Ellen S. Lathi, MD,”
and Dale J. Lange, MD’

A patient developed conjugate horizontal e y e deviation to the side opposite a large frontal-perisylvian
h e m o r r h a g e from a ruptured aneurysm. Autopsy
examination confirmed the hemispheric locus of the
h e m o r r h a g e and failed to disclose a n y lesion of the
brainstem or thalamus to explain the “wrong-way” e y e
deviation.
Pessin MS, Adelman LS, Prager RJ, Lathi ES, Lange DJ:
“Wrong-way eyes” in supratentorial hemorrhage.
Ann Neurol9:79-81, 1981

A p a t i e n t is described who had the unexpected
finding of c o n j u g a t e horizontal e y e deviation t o t h e
side opposite a large s u p r a t e n t o r i a l hemorrhage
(“wrong-way eyes”).

A hypertensive 57-year-old woman was transferred to N e w
England Medical Center Hospital in September, 1979, because of left hemiplegia. That morning she had developed a
severe occipital headache and stiff neck, immediately followed by weakness, sweating, diarrhea, nausea, and vomiting. At another hospital a left hemiparesis with eyes deviated to the left was noted.
At her admission, blood pressure was l90/110 m m H g
with a regular pulse of 98. H e r neck was supple. The
general physical examination was normal. The patient was
awake with her eyes open and blinking spontaneously, but
she did not respond to verbal instructions. H e r eyes deviated fully to the left in the horizontal plane, with no
observable nystagmus. Both oculocephalic testing and icewater caloric stimulation of the right external auditory
canal produced full horizontal conjugate eye excursion to
the right. Her pupils were 3 mm in diameter and reacted
normally to light stimulation. Visual threat from either side
produced a blink response. T h e optic discs were flat, and
retinal hemorrhages were not seen. Weakness of the left
lower face was present. T h e gag reflex was intact. T h e right
arm and leg moved spontaneously, and painful sternal rub
produced a purposeful response by the right hand but decerebrate posturing o n the left. O t h e r sensory modalities
could not be reliably tested. A flaccid, areflexic left hemi-

From the Departments of *Neurology, ?Pathology (Neuropathologyj, and $Radiology (Neuroradiology), Tufts-New England
Medical Center Hospital, 171 Harrison Ave, Boston, MA 02111.
Received Feb 20, 1980, and in revised form Apr 26. Accepted for
publication May 3, 1980.
Address reprint requests to Dr Pessin.

0364-5 134/81/0l0079-03$01.25 @ 1980 by the American Neurological Association

79

Fig 1. Axial nonenhanred C T scun at the level of the frontal
horns.

F i g 2. Section of the cerebral hemiJpheres in the plane ofthe
C T scan, showing the intvacerebral hemorrhage.

plegia was present. Plantar responses were extensor bilaterally.
A computed tomographic scan (Fig 1) demonstrated a
large area of hemorrhage in the right frontal and perisylvian
regions with compression of the right lateral ventricle and a
shift of midline structures to the left. Other scan slices
showed blood in the right lateral and fourth ventricles.
Her eyes remained conjugately deviated to the left, but
by afternoon both pupils were 4 mm in diameter and unreactive to light. Decerebrate posturing to minimal stimulation was present bilaterally. Her condition did not improve, and during the night she died.

into the frontal white matter from the subarachnoid
hemorrhage in the right sylvian fissure. It reached the
right frontal horn anterior to the basal ganglia and
dissected caudal to the thalamus. T h e thalamus was
not involved, and, although a small portion of the
caudal putamen was destroyed by the hemorrhage,
the rest of the basal ganglia were intact (Fig 2). A
small secondary midline hemorrhage was seen in
the midbrain, but the pons was not involved. Microscopic sections confirmed the gross findings. The
thalamus, pons, and basal ganglia (apart from the
caudal putamen) were normal histologically.

Neuropathological Findings
Recent subarachnoid hemorrhage was present over
the base of the brain, in the right sylvian fissure, and
over the convexity of the right cerebral hemisphere.
Three saccular aneurysms were found o n the intracerebral arteries. T h e largest (0.7 cm) was at the bifurcation of the right middle cerebral artery in the
sylvian fissure. A ragged tear measuring 0.3 cm in
longest dimension was present on the lateral aspect
of the sac, and this was presumed to be the source of
the hemorrhage. Small unruptured aneurysms were
found on both anterior cerebral arteries.
The brain was sectioned in the plane of the C T
scan. A crescentic hemorrhage was found extending

Discussion
It is well known that supratentorial hemorrhage may
produce contralateral hemiplegia with con jugate
horizontal eye deviation away from the paralysis and
toward the side of the lesion. By contrast, in a pontine lesion the eyes may conjugately deviate toward
the side of the hemiplegia.
In 1967, Fisher [l]first called attention to the occurrence of conjugate eye deviation to the “wrong”
side in supratentorial, hypertensive hemorrhage. He
reported three patients with pathologically proved
thalamic hemorrhage and a massive collection of
blood within the third ventricle whose eyes had
conjugately deviated away from the side of the lesion

80 Annals of Neurology Vol 9

No 1 January 1981

and toward the hemiplegia. No anatomical or physiological explanation for this finding was apparent.
Keane [3] later corroborated Fisher’s observation in
three patients with pathologically verified supratentorial hemorrhage, all involving the thalamus. More
recently [6] the same conjugate gaze abnormality was
reported in three of eighteen patients with thalamic
hemorrhage documented by CT scan. This uncommon gaze disorder has not been reported in association with hypertensive hemorrhage at other supratentorial sites [41, including the putamen 121.
In contrast to the other reported cases El, 3,61, our
patient had neither a hypertensive thalamic hemorrhage nor a massive collection of blood in the third
ventricle. H e r parenchymatous hemorrhage resulted
from rupture of a saccular aneurysm of the middle
cerebral artery and was associated with subarachnoid as well as intraventricular blood. However, the
parenchymal extension of the hematoma was a destructive mass lesion similar to a primary hypertensive hemorrhage.
We considered but dismissed several factors as the
cause for this patient’s gaze preference, including the
possibility that the hematoma had acted as an epileptic (irritative) focus, forcing the eyes in the opposite
direction. Although our patient did not have an electroencephalogram, no focal or generalized seizure
activity was observed in the limbs, and nystagmoid
jerking of the eyes-an expected feature of a frontal
cortex seizure focus [5]-was absent. Furthermore,
two of Keane’s patients (Cases 1 and 3 [31) had an
electroencephalogram during the period of their
conjugate gaze disorder, and only bilateral slowing
was observed. The pathological examination ruled
out the possibility that the patient’s conjugate leftward eye deviation resulted from an additional destructive lesion either in the left hemisphere or in the
pons. Thus, we can only document but cannot explain this observed conjugate gaze preference to the
unexpected side in association with a supratentorial
hemorrhage that spared the thalamus.
References

-

1. Fisher CM: Some neuro-oahthalmoLoeica1 observations. T
Neural Neurosurg Psychiatry 30:383-392, 1967
2. Hier DB, Davis KR, Richardson EP Jr, Mohr JP: Hypertensive
putaminal hemorrhage. Ann Neurol 1:152-159, 1977
3. Keane JR: Contralateral gaze deviation with supratentorial
hemorrhage. Three pathologically verified cases. Arch Neurol

32:119-122, 1975
4. Mohr JP, Caplan LR, Melski JW,
et al The Harvard Cooperative Stroke Registry: a prospective registry. Neurology 28:
754-762, 1978
5 . Walsh FB, Hoyt WF (eds): Topical diagnosis in the ocular
motor system. In Clinical Neuro-Ophthalmology. Third edition. Baltimore, Williams & Wilkins, 1969, vol 1, pp 208-209
6. Walshe TM, Davis KR, Fisher CM: ’Thalamic hemorrhage: a

computed tomographic-clinical correlation. Neurology (Minneap) 27:217-222, 1977

Postictal Pleocytosis
James W. Schmidley, MD, and Roger P. Simon, M D

Six patients showed a transient and otherwise unexplained cerebrospinal fluid (CSF) pleocytosis following
a flurry of generalized convulsions. Each had an obvious cause for repeated seizures. No evidence was found
for an infectious, inflammatory, neoplastic, or other
cause for the pleocytosis. All CSF specimens were clear
and colorless, under normal pressure, and bacteriologically sterile. The maximal leukocyte count ranged
from 9 to 80 per cubic millimeter and reached a maximum on the day after cessation of convulsions. NO
specimen contained more than 650 erythrocytes. Two
patients initially had a mildly increased CSF protein;
glucose values were unremarkable.
We propose that the pleocytosis in these patients was
a result of frequently repeated generalized convulsions. The mechanism of postictal pleocytosis is uncertain. It may result from transient breakdown of
the blood-brain barrier, which has been demonstrated
after seizures in experimental animals. Although infectious causes must first be considered and rigorously
searched for, it appears that seizures alone may cause a
transient CSF pleocytosis.
Schmidley JW, Simon RP: Postictal pleocytosis.
Ann Neurol 9231-84, 1981

Among a large number of patients admitted t o a city
hospital with repetitive generalized convulsions, we
have encountered six in whom the cerebrospinal fluid
(CSF) showed an otherwise unexplained mild, transient pleocytosis. While the occurrence of such postictal pleocytosis has occasionally been mentioned in
the literature [4, 5, 81, the phenomenon is not well
documented; its time course has not been reported in
detail [15].

Case Summaries
Patients 1, 2, and 3 were young, healthy people without a
history of tuberculosis or epilepsy, who took overdoses of
isonicotinic acid (INH) and were admitted after repeated
grand ma1 convulsions. All exhibited the profound metabolic acidosis characteristic of INH poisoning, and two
showed the typical hyperglycemia 111. Physical examinations and laboratory studies revealed no other pertinent abnormalities. When INH poisoning was suspected,
pyridoxine was administered. Two patients were given

From the Department of Neurology, University of California, San
Francisco, School of Medicine, 503 Parnassus Ave (794-M),
San
Francisco, CA 94141.
Received Apr 14, 1980, and in revised form June 2. Accepted for
publication June 7, 1980.

Address reprint requests to Dr Schmidley.

0364-5134/Sl/0100Sl-04$01.25 @ 1980 by the American Neurological Association

81