Hemiplegic Syndrome of the PosteriorCerebral ArteryBY D. FRANK BENSON, M.D., AND E. B. TOMLINSON, M.B., M.R.A.C.P.

Abstract:HemiplegicSyndromeof thePosteriorCerebralArtery

• An unusual syndrome is described consisting of right hemiplegia, righthemisensory loss, mild naming disturbance, and severe alexia coupled withnormal expressive language and ability to write. The clinical syndrome of alexiawithout agraphia strongly suggests involvement of the left posterior cerebralartery. A study of the territory of distribution of the posterior cerebral arterywould appear to confirm the possibility that occlusion of this vessel couldproduce the entire symptom picture. Of particular interest was the unusualhemiplegia, involving both limbs and face equally, but with a minimum ofspasticity.

ADDITIONAL KEY WORDSarterial occlusionhemianesthesia

agraphiacerebral infarction alexia

homonymous hemianopia

• Well-defined neurological syndromes pro-duced by discrete infarctions of the nervoussystem were first described in the latter part ofthe nineteenth century. At that time Huebner'sarteritis was common and most of thesesyndromes involved the brainstem. The uniquecombination of well-localized cranial nervenuclei and well-defined fibers of passageenabled discrete damage involving both sys-tems to be accurately localized clinically.Elsewhere within the central nervous systemsuch precision is rarely possible.

The cerebral hemispheres have a muchbetter collateral circulation, and less specificrelationship between structure and function,than has the brain stem. Thus, a hemisphericvascular lesion may produce no change, or avariety of neurological disabilities of varying

From the Aphasia Research Section, Boston VeteransAdministration Hospital, and the Neurology Depart-ment, Boston University School of Medicine (BostonVA Hospital, 150 South Huntington Avenue, Boston,Massachusetts, 02130).

This study was supported in part by Grant#NB06209 from the National Institute of Neurologi-cal Disease and Stroke to Boston University School ofMedicine.

Presented to the American Heart Association,Atlantic City, New Jersey, November 14, 1970.

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severity. Further, large-vessel disease mayresult in pathological lesions which, thoughextensive, appear clinically to be very limited.Both pathological studies and cerebral angiog-raphy have tended to create skepticism as tothe precise causal relationship between specificvascular involvement and specific symptoma-tology. Nevertheless, several vascular syn-dromes have been recognized, particularly theoccurrence of contralateral hemiplegia andaphasia following occlusion of the middlecerebral artery of the speech-dominant hemi-sphere.

We recently studied two patients whosuffered the sudden onset of right hemiplegia,hemianesthesia and homonymous hemianopiatogether with an aphasic disability. In thesepatients the lesion appeared to be a leftoccipital infarction, resulting not from involve-ment of the middle cerebral artery but of theposterior cerebral artery.

Case IA 53-year-old dispatch clerk was admitted to thehospital directly from his place of employmentfollowing the onset of a rapidly progressive righthemiparesis. For four days prior to admission hehad been aware of numbness involving the rightface and had suffered one episode of transientsyncope. There was a five-year history of known,

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untreated hypertension and a longer history ofexcessive ethanol intake.

On admission he was conscious but dis-oriented and mildly aphasic. There was a flaccidright hemiplegia, a right visual field defect andanesthesia to all sensory modalities on the rightside. Initial blood pressure was 140/85 but soonrose to 215/110. Tangent screen examinationdemonstrated a right homonymous hemianopiawith macular sparing. Pinprick on the right sidewas reported as only a vague sensation; othersensory modalities were not appreciated at all onthe right side. All sensory testing was normal onthe left. The hemiplegia remained hypotonic withonly slight flexor withdrawal from painful stimuli.The right tendon reflexes were brisker than theleft and the right toe sign was extensor.

The initial disorientation cleared rapidly andmultiple examinations of mental status throughthe remainder of the hospital stay revealed noabnormality. He was always fully alert andcooperative, aware of his hemiplegia although heappeared to underestimate the severity. He gave agood account of the illness and formal testingrevealed normal memory function. Conversationalspeech was fluent with normal grammaticalstructure but showed evidence of word-findingproblems. Comprehension of spoken language waseasily within normal limits. He had great difficultynaming objects, even common ones, on confronta-tion but invariably demonstrated that he recog-nized the object by manually or verballydemonstrating its use. He could spell out loud andimmediately recognized words spelled to him. Thehemiplegia precluded use of the right hand but heproduced legible writing with his left hand, bothto command and dictation. In contrast, he totallyfailed to interpret written language; he couldname a few individual letters but recognized nowords, not even his own name. He could readnumbers aloud and do arithmetic problems.Although he could draw, he showed considerableconstructional disturbance, particularly with blockdesigns. He had great difficulty with color names.While he could accurately match colored chips hecould neither name a color nor point to theappropriate color when the name was offered bythe examiner.

All blood, electrolyte, enzyme and liverfunction tests were consistently normal. X-rays ofskull and chest were normal. EEG revealed diffuseleft hemisphere slowing without focus. Radioiso-tope brain scan demonstrated increased uptake inthe left parieto-occipital area, seen most clearlyin the left midline aspect of the posterior view(fig. 1).COURSE

The blood pressure elevation was treated success-fully. Physical rehabilitation measures were rapid-

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ly followed by walking, at first with cane andbrace, but soon without either. Return of functionto the arm was slower and less complete but, incontrast to many hemiplegics, showed return ofconsiderable digital function and residual spastici-ty was very mild. Sensory appreciation improvedslowly. If urged he could hold a cup or shavehimself with the right hand, but if left to himselfhe invariably used the left for one-handed tasks.There was also some improvement in readingability, although this remained limited. Atdischarge he could not return to work but wasable to care for himself and an invalid wife.

Case 2A 54-year-old itinerant alcoholic, found uncon-scious in a hotel room, was admitted to a localhospital where examination revealed a righthemiplegia and hemisensory defect. He rapidlyregained consciousness, and additional examina-tion disclosed a right visual field defect, skewdeviation (right eye down and in) and mild word-finding difficulty when speaking.

FIGURE 1

Radioisotope brain scan (case 1). Note increased ac-tivity on lower left of PA view and in lower posterioraspect of lateral view.

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HEMIPLEGIC SYNDROME OF THE POSTERIOR CEREBRAL ARTERY

Ten days later he was transferred to theBoston VA Hospital, where general examinationdisclosed a thin, poorly nourished man with bloodpressure of 160/80 and surgical scars on theabdomen and left leg (sympathectomy and leftfemoral artery bypass). Tangent screen examina-tion demonstrated a dense right homonymoushemianopia with macular sparing. The skewdeviation persisted with the right eye laggingbehind on conjugate movements. There wasdistinct diminution of all sensory modalities onthe right side although some pain appreciationwas present. Paralysis was pronounced but withrelatively little spasticity. The tendon reflexes wereincreased and the right toe sign was extensor.

Orientation was full; speech was fluent withexcellent comprehension and repetition and onlymild difficulty when naming to confrontation.Colors were consistently misnamed although thepatient could match colors with ease. Reading wasextremely poor, limited to a few letters and a fewhigh-frequency words. In contrast he could write,spell aloud and recognize spelled words effortless-iy-

Laboratory tests such as blood, urine,

* *• »^«*• ••"•-•••'• •* •-

FIGURE 2

Radioisolope brain scan (case 2). Asymmetrical up-take similar to that seen in figure 1.

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electrolyte, enzyme, liver function and spinal fluidevaluations were all normal. X-rays were noncon-tributory. EEG showed leftsided slowing butwithout specific focus. An isotope brain scanrevealed increased activity in the posterior midlineextending to the left (fig. 2) suggesting involve-ment of the medial aspect of the left occipitallobe.

COURSE

The hospital course was characterized bynotable but incomplete improvement in alldisabilities. Thus, the hemiplegia cleared leavingonly a mildly spastic weakness in the right limbs.Sensory appreciation also improved but not tonormal and was intermittently aggravated bypainful dysesthesias involving much of the rightside. This latter finding improved with Dilantintherapy. Eye movements also improved althoughthe tendency for the right eye to lag remained.The hemianopia did not change but there wasimprovement in reading ability; he learned to readindividual letters, spell words out loud and thus"read" short phrases or sentences. The entirecourse was complicated by severe ischemia in theright lower extremity, finally necessitating rightfemoral artery surgery and amputation of severaltoes.

DiscussionThe first patient was originally thought to havean infarction involving a major portion of thedominant parietal lobe secondary to middlecerebral artery involvement. The diagnosis wasbased on the presence of fluent speech, grossdisturbances in reading ability and wordfinding associated with a rightsided paresis,sensory loss and homonymous hemianopia.Repeated evaluations, however, demonstratedthat he could recognize spelled words, couldspell out loud and with help could spell with apencil or anagram blocks but could not read.These features were even more fully developedin the second patient and suggested thesyndrome of alexia without agraphia. Bothpatients, however, were hemiplegic and had asensory loss, findings not classically associatedwith this syndrome.

Alexia without agraphia has long beenrecognized1-2 and, while not common, there isa remarkable consistency in both the clinicalfindings and the pathology.1^15 This syndrometypically has an acute onset with difficulty inreading, some unsteadiness and little else.Examination reveals a right homonymoushemianopia with macular sparing and totalinability to read; in contrast there is an almost

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normal ability to write, to spell out loud and torecognize spelled words. In addition, there isfrequently an inability to name a color or topoint to a color when the name is given, eventhough colors can be matched accurately. Thishas been called color agnosia.6 There are noother aphasic symptoms. The underlying pa-thology is infarction of the medial occipitalstructures (lingula, fusiform and calcarinecortex) plus infarction of the splenium of thecorpus callosum. Most often this has followedocclusion of the left posterior cerebral artery.Our patients had the alexia without agraphia,color agnosia and right homonymous hemi-anopia, clinical findings similar to the reportedcases.

Other findings in these cases, however, areatypical and need further consideration. Hemi-paresis is almost never reported in cases ofalexia without agraphia. This hemiparesisdiffered from that typically seen after hemi-spheric infarction in that the entire side wasinvolved (face, arm and leg) and the proximallimb was more impaired than the distal limb.The degree of spasticity was exceptionallymild, much less than usually recorded follow-ing either cortical or capsular infarction.Involvement of the pyramidal tracts at thepeduncular level has been shown to produce analmost nonspastic hemiplegia,7 probably be-cause at this point pyramidal and extrapyra-midal pathways are separate.8 Thus, a highbrain stem or diencephalic lesion would beconsistent with the hemiplegia in these cases.

Hemisensory loss is not usually reportedin alexia without agraphia. Originally, both ofour patients suffered profound sensory lossinvolving all modalities including pain. Thedistinct loss of pain suggested a deeply seatedlesion, at the level of the thalamus or below.Therefore both the motor and sensory distur-bances could be caused by selective infarctionin the diencephalic and mesencephalic regionswhich are fed by branches of the posteriorcerebral artery. This would also be consistentwith the usual etiology of alexia withoutagraphia.

Some of the other clinical observationsare more difficult to explain. The first patienthad a marked word-finding defect. Anomia(word-finding defect) is not readily localized inthe cortex, and in clinical practice an aphasicsyndrome consisting only of word-findingdifficulty cannot be localized.0 Among the

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many cortical areas occasionally linked withword-finding defect, one lies in the posteriorand inferior temporal region, Brodmann's area37.10 This area may receive blood from twosources, the posterior and the middle cerebralarteries. It seems possible that the posteriorcerebral artery could have provided most of thecirculation for this area and that occlusionproduced infarction which in turn affectedword finding.

Constructional disturbance usually indi-cates parietal abnormality and is most severewith biparietal involvement.11 Our patients hadno firm evidence of such lesions and otherexplanations can be considered. There arereports of patients without parietal abnormalitywho had definite constructional disturbance.These are the split brain patients12 whereconstructional performance was well belownormal, actually on the level of parietallydamaged patients. Is it possible that thecallosal damage postulated in our patients,infarction of the splenium, disturbed construc-tional capabilities by separating the twoparietal areas? This can only be conjectured.

FIGURE 3

Schematic view to emphasize some of the significantproximal branches of the posterior cerebral artery.

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HEMIPLEGIC SYNDROME OF THE POSTERIOR CEREBRAL ARTERY

HIPPOCAMPAL BRANCHES

FIGURE 4

Distal branches of posterior cerebral artery.

Radioisotope brain scans were performedto confirm the suspected localization. In ourinstitution these studies have been usedextensively and, when positive, are consideredgood indicators of the site of cerebral lesions.13

The scans were positive in both patients (figs.1 and 2), demonstrating increased isotopeactivity in the medial aspect of the occipitallobe and thus in agreement with the clinicallocalization. EEGs were performed on bothpatients. They did not show focal corticalchanges but did demonstrate slow wave activityinvolving the entire left hemisphere, possiblyan indication of more centrally located lesion.

The known distribution area of theposterior cerebral artery is consistent with theconjectured localization. Just after formationof the posterior cerebrals from the basilarartery a number of fine branches enter theanterolateral mesencephalon, particularly thearea of the cerebral peduncles. A number ofadditional branches from this area enter thethalamus (thalamo-perforating, thalamo-genicu-late, posterior choroidal) and provide circula-tion to the posterior thalamus (fig. 3). Beyondthis level a branch proceeds upward andmedially to the splenium of the corpuscallosum. A series of branches arch downward

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and then forward on the medial and inferiorsurface of the hippocampus (the hippocampalbranches) (figs. 3 and 4) and the main trunkproceeds posteriorly as the calcarine artery.Thus, occlusion of the left posterior cerebralartery just beyond the upper limits of thebasilar artery could produce the hemiplegia(peduncular branches), the sensory loss (tha-lamic branches), the homonymous hemianopia(calcarine branch), the alexia without agra-phia (calcarine branch plus splenial branch),the memory loss and anomia (hippocampalbranch).

The literature offers some support for thisconjecture. Foix and Masson14 postulated twosyndromes resulting from posterior cerebralocclusion: (1) a posterior syndrome withhomonymous hemianopia and alexia, and(2) an anterior syndrome with thalamicinvolvement producing a paresis, a profoundsensory loss, and, if on the dominant side, adisturbance in naming. They presented a singlecase with pathological evidence of bothanterior and posterior involvement but ratherinadequate clinical studies. They also men-tioned briefly a case report of Dejerine andThomas with clinical findings similar to thepresent patients and pathology limited to the

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distribution area of the posterior cerebralartery.

Whether this syndrome is as rare as thesefew reported cases would suggest is question-able. It is altogether too easy to consider thatthe hemiparesis and hemianesthesia indicate adisturbance in the territory of the middlecerebral artery, thus neglecting the existence ofa distinctly different syndrome. The desirabilityfor a proper diagnosis lies in the muchimproved outlook for rehabilitation measuresin the posterior cerebral cases. Motor andlanguage function appears to respond better toretraining efforts. The failure to recoversensory function, however, may provide amajor difficulty.

References1. Dejerine J : Contribution a l'6tude anatomo-

pathologique et clinique des differentes va-ne>£s de c£cit£ verbale. Mem Soc Biol 4 : 6 1 -90, 1892

2. Wylie J : The Disorders of Speech. Edinburgh,Oliver and Boyd, 1 894

3. Hinshelwood J, Mocphail A: A case of word-blindness with right homonymous hemianopsia.Brit Med J 2 : 1304-1307, 1904

4. Gloning I, Gloning K, Seitelberger F, et a l : EinFall von reiner Wortblindheit mit Obduktions-befund. Wien Z Nervenheilk 12: 194-215, 1955

5. Benson DF, Geschwind N: The alexias. InVinken PJ, Bruyn GW (eds) : Handbook of

Clinical Neurology (vol 4) . Amsterdam, NorthHolland, 1969

6. Rubens AB, Benson DF: Associative visualagnosia. Arch Neurol (Chicago) 24: 305-316,1971

7. Bucy PC, Keplinger JE: Section of thecerebral peduncles. In Yahr MD (ed) : TransAmer Neurol Assoc. New York, Springer, pp65-66, 1960

8. Crosby EC, Schneider RC, DeJong BR, et a l : Thealternations of tonus and movements through theinterplay between the cerebral hemispheres andthe cerebellum. J Comp Neurol Suppl 1 to 127:1-91, 1966

9. Gloning, I, Gloning K, Hoff H: Aphasia—aclinical syndrome. In Halpern L (ed) : Prob-lems of Dynamic Neurology. Jerusalem, He-brew University Press, pp 63-70, 1963

10. Nielsen JM: Agnosia, Apraxia and Aphasia—Their Value in Cerebral Localization (ed 2 ) .New York, Hafner, 1936

11. Warrington EK: Constructional apraxia. InVinken PJ, Bruyn GW (eds) : Handbook ofClinical Neurology (vol 4 ) . Amsterdam, NorthHolland, 1969

12. Gazzaniga M, Bogen JE, Sperry RW: Observa-tions on visual perception after disconnexionof the cerebral hemispheres. Brain 88: 221 -236, 1965

13. Benson DF, Patten DH: The use of radioactiveisotopes in the localization of aphasia-produc-ing lesions. Cortex 3: 258-271, 1967

14. Foix, C, Masson A : Le syndrome de I'arterecerebrale poste>ieure. Presse M6d (Paris) 32:361-365, 1923

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D. Frank BENSON and E. B. TOMLINSONHemiplegic Syndrome of the Posterior Cerebral Artery

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1971 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.2.6.559

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