Unilateral Oculomotor Palsy and Bilateral Ptosis From Paramedian Midbrain Infarction Grant T. Liu, MD; Enrique J. Carrazana, MD; Michael E. Charness, MD

\s=b\ Lesions of the oculomotor fascicles are localized clinically by associated neurologic deficits. We present two patients with bilateral ptosis, unilateral paresis of all other muscles innervated by the oculomotor nerve, and sparing of the contralateral superior rectus muscle\p=m-\findingssuggesting a lesion of the proximal oculomotor fascicles and the central caudal subnucleus. To our knowledge, these are the first such cases with radiologic confirmation of a lesion within the dorsal, paramedian midbrain. (Arch Neurol. 1991 ;48:983-986)

^Phe oculomotor fascicles sweep ventrally and laterally from the oculo¬ motor complex, pass through and medi¬ al to the red nucleus, and converge to exit the brain stem medial to the cere¬ bral peduncles.1 The clinical localization of lesions along the dorsal-ventral course of the oculomotor fascicles relies on associated neurologic findings. Dam¬ age to the ventral fascicles and the near¬

by cerebral peduncle causes ipsilateral third-nerve palsy and contralateral he¬ miparesis (Weber's syndrome).2 In¬

volvement of fascicles within the red nucleus leads to oculomotor palsy with contralateral involuntary movements (Benedikt's syndrome). Extension of such a lesion to the brachium conjunctivum produces additional contralateral ataxia (Claude's syndrome).2 When suf¬ ficiently small, fascicular lesions can mimic complete or partial extra-axial third-nerve palsies.3"8 Most of these have been located in the ventral mid¬ brain, sparing the red nucleus and cere¬ bral peduncles. Small lesions of the proximal oculo¬ motor fascicles have been reported only rarely.0,8 Extension of such a lesion would involve the oculomotor subnu¬ clei, the medial longitudinal fasciculus, Accepted for publication April 5,1991. From the Department of Neurology, Harvard Medical School; Division of Neurology, Brigham and Women's Hospital; Section of Neurology, Brockton-West Roxbury Veterans Affairs Medical Center; the Harvard-Longwood Neurology Training Program, Boston, Mass. Reprint requests to the Section of Neurology (127), Brockton-West Roxbury Veterans Affairs Medical Center, 1400 VFW Pky, West Roxbury, MA 02132 (Dr Charness).

and the

mesencephalic reticular forma¬

tion, causing ipsilateral oculomotor pa¬ resis and combinations of bilateral pto¬ sis, bilateral superior rectus palsy,

internuclear ophthalmoplegia, and leth¬ argy.29 We present two patients in whom focal infarction ofthe dorsal, par¬ amedian midbrain led to a unique syn¬ drome of pupil-sparing oculomotor pal¬ sy, lethargy, and bilateral ptosis, without affecting the contralateral su¬

perior rectus.

REPORT OF CASES CASE 1.—A 46-year-old man developed double vision, bilateral ptosis, and lethargy immediately after a percutaneous translu¬ minal coronary angioplasty for a complete right coronary artery occlusion. The patient had a history of recent myocardial infarction and hypercholesterolemia. Examination re¬ vealed pronounced bilateral ptosis in the set¬ ting of mild inattention and drowsiness. He could open his eyes only by lifting his lids manually. Visual acuity with correction was JI OD and J2 OS. Visual fields by confronta¬ tion were normal. A small cotton wool exú¬ date was noted along the superotemporal ar¬ cade in the left fundus. The pupils were equal, round, and reactive to light. In prima¬ ry position the left eye deviated outward and downward. There was markedly decreased adduction and elevation of the left eye, and downward gaze was diminished on abduc¬ tion. Attempted adduction ofthe left eye was accompanied by abducting nystagmus of the right eye. All movements of the right eye were normal. The remainder of his neurolog¬ ic examination was normal. Magnetic reso¬ nance imaging (48 hours after the event) showed a small focus of increased T2 signal in the left periaqueductal gray matter overlap¬ ping the left medial longitudinal fasciculus and caudal third-nerve nucleus (Fig 1). Two small punctate foci of increased T, signal were seen in the deep white matter of the right parietal and frontal lobes. Over the first 48 hours right-sided ptosis resolved and left-sided ptosis improved con¬ siderably. Four days after the event he showed left-sided ptosis and diminished function ofthe left medial, superior, and infe¬ rior rectus and inferior oblique muscles with normal eye movements on the right side, except for abducting nystagmus on right hor¬ izontal gaze (Fig 2). Abduction and elevation of the left eye improved gradually over the subsequent week. After 6 weeks he had dip¬ lopia with occasional fused vision, mild left-

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sided ptosis with superior and medial rectus paresis, and a mild left-sided internuclear ophthalmoplegia. One month later transient diplopia was present only on sudden upgaze or

with fatigue. CASE 2.—A

31-year-old, previously healthy woman came to the hospital on Janu¬ ary 16, 1990, complaining of sudden dizzi¬ ness, difficulty seeing, and droopy eyelids. She smoked cigarettes and took oral contra¬ ceptives. Her blood pressure was 110/80 mm Hg and her heart rate was 60 beats per min¬ ute and regular. There were no heart mur¬ murs. She was drowsy and inattentive but easily arousable. Her visual fields and acuity were normal. There was bilateral ptosis, which was worse on the left side. In primary position the left eye deviated outward and downward. Movements of the right eye were normal without abducting nystagmus. The left eye could not adduct and had only 30° of upward gaze and 45° of downward gaze. The pupils were 2 mm bilaterally and briskly re¬ active to light. She had mild right face and arm weakness, right-sided hyperreflexia, and truncal as well as gait ataxia. The hematocrit, erythrocyte sedimenta¬ tion rate, prothrombin time, partial thromboplastin time, and protein C, protein S, and antithrombin III levels were all normal. Re¬ sults of laboratory studies revealed that the cerebrospinal fluid contained the following IO9/values: white blood cells, 0.006 (6/mm3) ( lymphocytes, 0.91 [91]; mononu¬ clear leukocytes, 0.05 [5]); red blood cells, 1 1012/L (1/mm3); glucose, 3.4 mmol/L (62 mg/dL); and protein 0.46 g/L (46 mg/dL). Rapid plasma reagin and antinuclear anti¬ body were negative. Echocardiogram and 24-hour Holter monitor were normal. Mag¬ netic resonance imaging 1 day after the event demonstrated three foci of increased T2 sig¬ nal in the left side ofthe midbrain: one located in the periaqueductal gray, one lateral to the red nucleus, and the third in the lateral por¬ tion of the cerebral penduncle (Fig 3). She was much more alert 2 days after admission. One week later, right-sided ptosis had re¬ solved almost completely, left vertical gaze was improved, but she still showed mild leftsided ptosis and had only 10° of adduction. COMMENT

Both patients had focal infarcts ofthe dorsal midbrain in the territory of the perforating paramedian branches ofthe proximal posterior cerebral artery (mesencephalic artery).9,10 Biller and

colleagues"

described

a man

who,

like

patient 1, developed a midbrain stroke after percutaneous transluminal coro¬

angioplasty. In Dawson and Fi¬ scher's12 review of the neurologic com¬ nary

plications of cardiac catheterization, five of 10 affected patients developed pontine and mesencephalic dysfunction, most likely as a result of artery-to-ar¬ tery embolization. They postulated that

catheter-induced trauma to the aorta or to the origin ofthe vertebral, inominate, or subclavian arteries might cause em¬ bolization preferentially to the verte-

brobasilar circulation. Patient 1 had evi¬ dence for embolization in both the anterior and posterior circulations, in¬ volving the midbrain, retina, frontal lobe, and parietal lobe. Patient 2 likely suffered a thrombotic stroke as a conse¬ quence of her use of oral contraceptives and cigarettes, two additive risk factors for thrombosis.13 The sudden onset of symptoms, improvement within days, and cerebrospinal fluid profile were con¬ sistent with infarction, and a search for other causes, short of angiography, was

unrevealing.

Fig

1. —Magnetic resonance imaging (TR 2000 milliseconds, TE 80 milliseconds) of the midbrain in patient 1, 2 days after his infarct. A single area of increased T2 signal (arrow) Is seen In the left paramedian midbrain involving the caudal portion of the oculomotor nucleus, the medial longitudinal fasciculus, and the periaqueductal gray matter.

Fig

=

=

Fig 3. —Magnetic resonance Imaging (TR 2000 milliseconds; TE 80 milliseconds) of the midbrain in patient 2, 1 day after her Infarct. Three discrete regions of increased T2 signal are seen. The left paramedian lesion (arrow) is nearly identical to that of patient 1 (Fig 2). Additional lesions in the left lateral peduncle and lateral to the red nucleus should spare fhe third-nerve fascicles, which course through and medial to the red nucleus before exiting the brain stem in the ¡nterpeduncular fossa. =

=

2. —Eye movements In

patient 1,

4

days

after his infarct. All of the abnormalities are in the left eye, Including ptosis, diminished eleva¬ tion on right and left upward gaze, and mildly diminished adduction and depression. By this time the right-sided ptosis had resolved and the left-sided ptosis, adduction, and depression had improved considerably.

Fig 4.—Anatomy of the oculomotor complex, as proposed by Warwick." The superior rectus (SR) muscle is Innervated by a contralateral subnucleus. The central caudal nucleus (CCN) innervates both levator palpebrae muscles. The Edinger-Westphal subnucleus (E-W) and subnuclei for the inferior rectus (IR), Inferior oblique (10), and medial rectus (MR) muscle are arranged ipsilaterally. SO indicates superior oblique; LR, lateral rectus; and nuclei of the fourth (IV) and sixth (VI) cranial nerves (reproduced from reference 20 as modified from Warwick,14 with permission from Wiley-Liss).

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Ocular findings in these two patients confined to extraocular muscles innervated by the left third nerve: supe¬ rior, medial, and inferior rectus, inferi¬ or oblique, and levator palpebrae. In both cases, ptosis was bilateral and were

asymmetric, being worse ipsilateral to the ophthalmoparesis. The pupils were spared and all movements of the right

eye were normal to bedside examina¬ tion. (It is conceivable that minor in¬ volvement of the right superior rectus muscle might have been detected using more sensitive methods, such as Lan¬ caster testing.) Within 1 week, both pa¬ tients showed only left-sided abnormali¬ ties, including ptosis, decreased elevation, and impaired adduction, the latter due to an internuclear ophthalmo¬ plegia in patient 1 and a medial rectus palsy in patient 2. The selective involvement of oculo¬ motor function and the relative paucity of additional neurologic signs suggests that both patients suffered small lesions of the paramedian midbrain. Bilateral ptosis is the hallmark of involvement of the central caudal subnucleus and local¬ izes the lesions to the caudal oculomotor complex and its immediate vicinity.2,14"" The preservation of pupillary function implies sparing of the Edinger-Westphal complex and serves to delimit the dorsal and rostral extent of the nuclear lesion. " The internuclear ophthalmople¬ gia in patient 1 indicates involvement of the left medial longitudinal fasciculus, adjacent to the oculomotor complex, and drowsiness in both patients could be explained by transient disconnection of the midline midbrain reticular forma¬ tion from the thalamus.9 This clinical neuroanatomic localiza¬ tion was confirmed by magnetic reso¬ nance imaging, which disclosed a small lesion in the dorsal paramedian mid¬ brain in each patient. Although patient 2 had two additional lesions in the ven¬ tral midbrain, it is doubtful that these contributed significantly to her oculo¬ motor deficit since both were lateral to the third-nerve fascicles.] The lesion in¬ volving the left cerebral peduncle likely explains her right hemiparesis, where¬ as that lateral to the left red nucleus could have caused her ataxia by inter¬ rupting fibers from the superior cere¬ bellar peduncle in the dentatorubrothalamic tract.18,19 According to Warwick's14 scheme for the subdivisions of the oculomotor nu¬ clei, the midline central caudal nucleus supplies both levator palpebrae mus¬ cles, and each superior rectus muscle is innervated by a contralateral subnu¬ cleus (Fig 4). Ipsilateral subnuclei sub¬ serve the remaining extraocular mus¬ cles innervated by the third nerve and '

the parasympathetic pupillary constric¬ tor fibers.14,20 Bienfang21 demonstrated that axons from each superior rectus subnucleus cross the midline and pass through the contralateral subnucleus before reaching the opposite third nerve. Unilateral lesions of the oculo¬ motor complex should therefore cause bilateral ptosis, ipsilateral mydriasis, ipsilateral palsy of the medial rectus, inferior rectus, and inferior oblique muscles, and bilateral superior rectus

palsy.2,11,17,21"23

A small number of patients have been described in whom dorsal paramedian midbrain lesions have caused bilateral ptosis and ipsilateral oculomotor pare¬ sis.15,16,22"24 When present, involvement of the superior rectus has been either bi¬ lateral, from a nuclear lesion,16,22,23 or contralateral, from a supranuclear le¬ sion.24 Our patients are unique because oculomotor paresis and bilateral ptosis were unaccompanied by significant in¬ volvement of the contralateral superior rectus muscle. Although Caplan20 brief¬ ly mentioned two patients with bilateral

ptosis, complete ophthalmoplegia on one side, and "(no) other signs of third nerve deficit" on the other side, there was neither radiologie nor pathologic confirmation of the suspected midbrain

lesion. How could a lesion ofthe dorsal para¬ median midbrain produce bilateral pto¬ sis and ipsilateral elevator palsy? The central caudal and superior rectus subnuclei are adjacent structures.14 If the elevator palsy, like the bilateral ptosis, was caused by a nuclear lesion, then the superior rectus subnucleus would have to have been uncrossed, contradicting anatomic studies in several mammalian species.14,21,26"28 More likely, the elevator palsy was supranuclear or infranuclear. Ipsilateral29 and contralateral24,30 mid¬ brain lesions have been reported to

monocular, supranuclear paresis elevation, presumably by interrupt¬ ing axons from the rostral interstitial nucleus of the medial longitudinal fas¬ ciculus, which is believed to mediate up¬ gaze.29 However, in our patients, pare¬ sis of the superior rectus and inferior oblique muscles was distinguished by hypotropia in primary gaze, typically absent in a supranuclear lesion.29 Hence, the most likely explanation for their ipsilateral elevator palsy is a lesion cause

of

in the oculomotor fascicles. The pattern of recovery suggests that the major damage was infranuclear; contralateral ptosis resolved within a few days, leav¬ ing unilateral ptosis and ipsilateral ele¬ vator palsy (Fig 2). These findings sup¬ port the proposal that axons destined

for the superior rectus, inferior oblique, and levator palpebrae muscles segre-

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gate dorsolaterally within the oculomo¬ tor fascicles.1,7,31

Precise anatomic correlation of this oculomotor disorder ultimately re¬ quires postmortem examination. None¬ theless, the nearly identical clinical and magnetic resonance findings in these two patients delineate a new syndrome of the proximal oculomotor fascicles. The sudden onset of lethargy, bilateral ptosis, and ipsilateral third-nerve pal¬ sy, with sparing of the contralateral su¬ perior rectus should suggest a lesion of the dorsal paramedian midbrain, includ¬ ing the proximal oculomotor fascicles and the adjacent central caudal subnucleus. We are grateful to Don Bienfang, MD, Brigham and Women's Hospital, Boston, Mass, for helpful discussions and critical review ofthe manuscript.

References O, Johnson LN, Mamourian AC. Isolated inferior oblique paresis from brain-stem infarction: perspective on oculomotor fascicular organization in the ventral midbrain tegmentum. Arch Neurol. 1990;47:235-237. 2. Miller NR. Walsh and Hoyt's Clinical Neuro\x=req-\ ophthalmology. 4th ed. Baltimore, Md: Williams & Wilkins; 1985:657-663. 3. Nadeau SE, Trobe JD. Pupil sparing in oculo1. Castro

motor

palsy:

a

brief review. Ann Neurol.

1983;13:143-148.

4. Keane JR. Isolated brain-stem third

nerve

palsy. Arch Neurol. 1988;45:813-814. 5. Ksiazek SM, Repka MX, Maguire A, et al. Division oculomotor nerve paresis caused by intrin-

sic brainstem disease. Ann Neurol. 1989;26:714\x=req-\ 718. 6. Collard M, Saint-Val C, Mohr M, Kiesmann M. Paralysie isol\l=e'\edu nerf moteur oculaire commun par infarctus de ses fibr\l=e`\sfasciculaires. Rev Neurol. 1990;146:128-132. 7. Hriso E, Miller A, Masdeu JC. Monocular elevation weakness and ptosis: an oculomotor fascicular syndrome? Neurology. 1990;40(suppl 1): 309-310. 8. Hopf HC, Gutmann L. Diabetic 3rd nerve palsy: evidence for a mesencephalic lesion. Neurology. 1990;40:1041-1045. 9. Segarra JM. Cerebral vascular disease and behavior, I: the syndrome of the mesencephalic artery (basilar artery bifurcation). Arch Neurol.

1970;22:408-418. 10. Sieben G, De Reuck J, Vander Eecken H. Thrombosis of the mesencephalic artery: a clinico-

pathological study of two cases and its

correlation with the arterial vascularisation. Acta Neurol Belg.

1977;77:151-162. 11. Biller J, Shapiro R, Evans LS, Haag JR,

Fine M. Oculomotor nuclear complex infarction: clinical and radiological correlation. Arch Neurol.

1984;41:985-987. 12. Dawson DM, Fischer EG. Neurologic

plications

of cardiac catheterization.

1977;27:496-497.

com-

Neurology.

13. Longstreth WT, Swanson PD. Oral contraceptives and stroke. Stroke. 1984;15:747-750. 14. Warwick R. Representation of the extra-

ocular muscles in the oculomotor nuclei of the mon-

key. J Comp Neurol. 1953;98:449-495. 15. Stevenson GC, Hoyt WF. Metastasis to midbrain from mammillary carcinoma. JAMA.

1963;186:514-516. 16. Growdon JH, Winkler GF, Wray SH. Mid-

brain ptosis: a case with clinicopathologic correlation. Arch Neurol. 1974;30:179-181. 17. Miller NR. Walsh and Hoyt's Clinical Neuro-ophthalmology. 4th ed. Baltimore, Md: Wil-

liams & Wilkins; 1985:568-570. 18. Carpenter MB. Functional relationships between the red nucleus and the brachium conjunctivum: physiologic study of lesions of the red nucleus in monkeys with degenerated superior cerebellar brachia. Neurology. 1957;7:427-437. 19. Felice K, Keilson GR, Schwartz WJ. 'Rubral' gait ataxia. Neurology. 1990;40:1004-1005. 20. Glaser JS, Bachynski B. Infranuclear disorders of eye movement. In: Glaser JS, ed. Neuro\x=req-\ ophthalmology. Philadelphia, Pa: JB Lippincott; 1990:363. 21. Bienfang DC. Crossing axons in the third nerve nucleus. Invest Ophthalmol. 1975;14:927\x=req-\ 931. 22. Bogousslavsky J, Regli F. Nuclear and pre-

nuclear syndromes of the oculomotor nerve. Neuro-

ophthalmol. 1983;3:211-216.

23. Zackon DH, Sharpe JA. Midbrain paresis of horizontal gaze. Ann Neurol. 1984;16:495-504. 24. Bogousslavsky J, Regli F, Ghika J, Hungerbuhler JP. Internuclear ophthalmoplegia, prenuclear paresis of contralateral superior rectus, and bilateral ptosis. J Neurol. 1983;230:197-203. 25. Caplan LR. Ptosis. J Neurol Neurosurg

Psychiatry. 1974;37:1-7.

26. Buttner-Ennever JA, Grob P, Akert K. A transsynaptic autoradiographic study of the pathways controlling the extraocular eye muscles, using [125I]B-IIb tetanus toxin fragment. Ann N Y Acad

Sci. 1981;374:154-170. 27. Porter JD, Guthrie BL,

Sparks DL.

Inner-

vation of monkey extraocular muscles: localization of sensory and motor neurons by retrograde transport of horseradish peroxidase. J Comp Neurol.

1983;218:208-219.

28. Gacek RR. Localization of neurons supplythe extraocular muscles in the kitten using horseradish peroxidase. Exp Neurol. 1974;44:381\x=req-\ 403. 29. Ford CS, Schwartze GM, Weaver RG, Troost BT. Monocular elevation paresis caused by an ipsilateral lesion. Neurology. 1984;34:1264-1267. 30. Lessell S. Supranuclear paralysis of monocular elevation. Neurology. 1975;25:1134-1136. 31. Abdollah A, Francis GS. Intraaxial divisional oculomotor paresis suggests intraaxial fascicular organization. Ann Neurol. 1990;28:589-590.

ing

Marchiafava-Bignami Disease, Syndrome of Interhemispheric Disconnection, and Right-handed Agraphia in a Left-hander A.

Rosa, MD; M. Demiati, MD; L. Cartz, MD; J. P. Mizon, MD

\s=b\ We present an original case of Marchiafava-Bignami disease in a 47-year-old left\x=req-\ handed alcoholic man. Computed tomography and magnetic resonance imaging demonstrated the typical lesion, a necrosis of the middle portion of the corpus callosum. Diagnosis may thus be established in the living. In our case, the course was not fatal, which, to our knowledge, has only been de-

scribed in four other

cases

in the literature.

Clinically, our patient demonstrated an interhemispheric disconnection syndrome. The striking feature is that some of the symptoms were on the side opposite of the one that has previously been described in the literature, eg, right-handed agraphia, while others were usual side, eg, left-handed anomia. We discuss cerebral dominance for speech and handedness in left-handers and come to the conclusion that our patient's clinical features can only be explained by right hemispheric dominance for handedness and bilateral hemispheric representation of on the

speech. (Arch Neurol. 1991 ; 48:986-988) disease is an 1\/ archiafava-Bignami uncommon disorder associated with alcoholism, presumably of nutri¬ tional or metabolic origin. This disease is defined by its pathologic features, ie, a symmetrical demyelination ofthe mid¬ dle portion ofthe corpus callosum, with

Accepted for publication March 25,1991. From the Service de Neurologie, Centre Hospitalier Regional et Universitaire d'Amiens (France).

Reprint requests to Service de Neurologie, H\l=o^\pital Nord, Place Victor Pauchet, BP 3006, 80030 Amiens, France (Dr Rosa).

or

without necrosis. The clinical fea¬

tures of the disease

and

diagnosis

was

quite variable, rarely made before are

postmortem examination until comput¬

ed tomography and magnetic resonance imaging were introduced. In some cases, the diagnosis is suggested by a syndrome of interhemispheric discon¬ nection.14 The course of the disease is usually fatal, yet we found four cases of recovery in the literature.30 We report the case of a left-handed alcoholic patient with Marchiafava-Bignami disease. The patient recovered, and special testing revealed an inter¬ hemispheric disconnection syndrome characterized by right-handed agraphia and apraxia, a sign of the foreign hand on the right side, and left-handed anomia. REPORT OF A CASE

54-year-old left-handed male alcoholic found unconscious at his home and was admitted to the hospital. Since his wife had left home 8 weeks previously, he had eaten very little but had continued drinking. Gen¬ eral physical examination revealed malnu¬ trition. The patient was confused and disori¬ ented as to time and space. Neurologic ex¬ amination revealed ataxia and gegenhalten. The ankle reflexes were abolished. There was no motor or sensory deficit. Plantar re¬ flexes were flexor. No ocular motor distur¬ bances were noted. The results of routine laboratory tests were normal. A cranial com¬ puted tomographic scan with and without contrast medium showed abnormal hypodensity of the corpus callosum, extending from the genu to the splenium; there was no con¬ trast enhancement. The patient received thi¬ amine treatment, and within a week he had A

was

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partially recovered:

consciousness

was nor¬

mal, and the ataxia and gegenhalten had dis¬ appeared. Cranial magnetic resonance imag¬ ing was performed on day 15 (Fig 1). A low-

signal intensity area was demonstrated in the corpus callosum, extending from the genu to the splenium in Trweighted images. In T2-weighted images, the abnormal area was

demonstrated

as a

high-intensity

area,

which extended beyond the corpus callosum into the hemispheric white substance of the frontal horns. Neuropsychological testing was performed; then the patient was trans¬ ferred to a convalescence ward. Six months later, a second series of neuropsychological tests were performed. A detailed account of his cognitive deficits is given below. A new computed tomographic scan showed the same abnormalities. Cerebral blood flow studies were performed with technetium Tc 99m exametazime and the scintillation cam¬ era. Several areas of decreased perfusion were demonstrated: the posterior zone ofthe frontal lobe and the parietal lobe ofthe right hemisphere; the temporo-occipital area of the left hemisphere; and the right cerebellum hemisphere with cerebellum diaschisis. NEUROPSYCHOLOGICAL FINDINGS

The patient was tested once he had recovered normal consciousness. The results were as follows: 1. Spontaneous speech was intact. Comprehension of verbal or written ma¬ terial was good. When asked to write, under dictation, spontaneously, or copying, the patient performed well with his left hand, but was unable to draw letters or words with his right hand (apraxie agraphia) (Fig 2). Draw¬ ing geometric figures was disturbed with both the left and the right hands

(constructional apraxia).

Unilateral oculomotor palsy and bilateral ptosis from paramedian midbrain infarction.

Lesions of the oculomotor fascicles are localized clinically by associated neurologic deficits. We present two patients with bilateral ptosis, unilate...
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