983

Pure Sensory StrokeClinical-Radiological Correlates of 21 Cases

Jong Sung Kim, MD

Background: Although pure sensory stroke is a relatively common lacunar syndrome, the responsiblelesions are often unidentified because of their small size. I reported 21 cases of pure sensory stroke inwhich the lesions could be identified by head computed tomography and/or magnetic resonance imagingand correlated the clinical findings with the radiological lesions.

Summary of Report: Eleven patients had thalamic strokes. Lacunes confined to the posterolateral partof the thalamus were found in nine cases, and hemorrhages of relatively large size were found in two. Fivepatients showed a loss of all sensory modalities, but six with very small lacunes showed minor or restrictedsensory changes. Seven patients with lacunes or hemorrhages in the lenticulocapsular region or coronaradiata showed abnormalities of spinothalamic tract sensation. Two patients with a small lacune and ahemorrhage in the pontine tegmentum showed a selective sensory deficit of the medial lemniscal type. Onepatient with a small cortical infarct showed a cortical sensory loss that was preceded by cortical sensorytransient ischemic attacks.

Conclusions: Pure sensory stroke can occur with lesions in various areas of the somatosensory system.Hemisensory deficits of all modalities usually are associated with a relatively large lacune or hemorrhagein the lateral thalamus, whereas tract-specific or restricted sensory changes suggest very small strokes inthe sensory pathway from the pons to the parietal cortex. (Stroke 1992;23:983-987)

KEY WORDS • computed tomography • magnetic resonance imaging • pure sensory stroke

Pure sensory stroke (PSS) is a well-defined clinicalentity in which hemisensory symptoms predom-inate without other major neurological signs.1

While Fisher2 reported PSS to be the most commonlacunar syndrome, more recent studies showed that it isthe second or fourth most common.34 Although tha-lamic stroke is the most frequent cause of PSS, nontha-lamic strokes involving the brain stem,5-16 internal cap-sule,17-20 or cerebral cortex21 are also reported toproduce PSS.

Because of their small sizes, the lesions producingPSS are often difficult to identify. Fisher22 previouslyanalyzed the clinical features of 135 patients with PSSand allied conditions but could not localize the lesions.Although computed tomography (CT) may be help-ful,23"25 it is often unable to confirm lesions.4-11'20'26 Withthe advent of magnetic resonance imaging (MRI), smallstrokes causing PSS are more easily identified. How-ever, until recently there has been no clinical-radiolog-ical study of PSS, which prompted me to report 21 casesin which clinical manifestations correlated with radio-logical (CT and/or MRI) findings.

Subjects and MethodsI identified 24 patients with pure hemisensory stroke

who showed appropriate lesions on head CT (GE/9800)and/or MRI at Asan Medical Center between Septem-

From the Department of Neurology, College of Medicine,University of Ulsan, Asan Medical Center, Seoul, Korea.

Address for correspondence: Jong Sung Kim, MD, Departmentof Neurology, Asan Medical Center, 388-1, Poongnap Dong,Songpa-Ku, Seoul 138-040, Korea.

Received January 1, 1992; accepted March 3, 1992.

ber 1989 and December 1991. The MRI studies wereperformed using a 1.5-T superconducting magnet (GE).Axial T2-weighted (repetition time/echo time [TR/TE],2,500/80), Tl-weighted (TR/TE, 600/20), and sagittalTl-weighted scans were generated with a slice thicknessof 5 mm. Three patients had more than one lesioncontralateral to the sensory deficit and were thus ex-cluded. All 21 patients were examined by the author(patients 12 and 19 were previously reported16-20). In 14patients CT identified the lesions. In four of thesepatients MRI was performed later to confirm the pres-ence of the lesion and the absence of other lesions,whereas only MRI was performed in seven patients. Theclinical symptoms and signs were correlated with theradiological localization. The size of the stroke wasclassified as large, small, or very small when the longestdiameter of the lesion was > 1.5 cm, 0.5-1.5 cm, or <0.5cm, respectively.

ResultsTwenty-one patients (12 men and 9 women, aged

46-74 [mean, 57] years) were studied; the details ofeach patient are summarized in Table 1. Risk factors forstroke included hypertension in 16, diabetes mellitus inthree, and hyperlipidemia in three. Patient 2, who hadcoronary heart disease, was positive for both lupusanticoagulant and anticardiolipin antibody, and patient3 had pancreatic cancer.

Thalamic StrokesEleven patients (cases 1-11) had thalamic strokes, of

which nine were ischemic (lacune) and two were hem-orrhagic. Eight lesions were demonstrated by head CT

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984 Stroke Vol 23, No 7 July 1992

TABLE

Case

1. Clinical

Sex/Age

Features of 21

Riskfactors

Patients With

Nature

Pure Sensory

Site

Stroke

Size Pi

Sensory

T V

deficits

Po C Identification Remark

1

2

3456

7

8

9

10

11

12

13

14

15

16

17

18

19

20

21

F/52

M/55

M/55

M/52

F/58

M/55

M/50

F/64

F/57

M/56

M/46

M/47

M/56

M/61

M/55

M/55F/59F/55F/67F/74

F/65

HTCHD, APLCancerHTHTHT

HT, DM

HT

HT

DM

HT

HT, HLHTHTHTHTHTHLHTHTDM, HL

III

HH

I

I

I

I

I

I

IIH

HII

I

HII

RThalLThalRThalLThalLThalRThal

LThal

RThal

RThal

RThalLThal

L Post ICR Post ICL Post ICL Post ICL C R

L C R

L C R

R PonsR PonsR Parietal

SS

sLLVS

VS

VS

VS

VS

VS

VS

sVS

VS

VS

sVS

VS

ss

+-nc

+nc

nc

_

_

—

-_

-

-

-

-

-

-

-

-

-

+

CTCT

CT

CT

CT

CT

MRI

CT

MRI

MRI

CT

CT, MRICT

MRI

MRI

CT, MRICTMRICT, MRICT, MRIMRI

FaciobrachialdistributionFaciobrachialdistributionCheiro-oralsyndromeCheiro-oraland four toes

Restricted todigits

Sensory TIA

Sensory TIA

Pi, pinprick; T, touch; V, vibration; Po, position; C, cortical; F, female; M, male; HT, hypertension; CHD, coronary heart disease; APL,antiphospholipid antibody syndrome; DM, diabetes mellitus; HL, hyperlipidemia; I, infarct; H, hemorrhage; R, right; L, left; Thai, thalamus;Post, posterior; IC, internal capsule; CR, corona radiata; S, small; L, large; VS, very small; nc, not checked; CT, computed tomography;MRI, magnetic resonance imaging; TIA, transient ischemic attack.

and three by MRI. In all ischemic strokes, the lesionswere confined to the posterolateral part of the thalamusprobably involving the ventral posterolateral nucleus(Figure 1). The two hemorrhagic strokes were relativelylarge in size.

Five patients with thalamic stroke showed sensorydeficit of both spinothalamic and medial lemniscaltypes, whereas six with very small lacunes (cases 6-11)did not. Patients 6 and 7 complained of an unpleasantnumbness over the face and arm without an objectivesensory deficit, while patient 10 showed a mildly de-creased pinprick sense only. Patient 8, who had de-creased pinprick and vibration senses restricted over theleft perioral and cheek area, suffered numbness in thoseareas as well as the hard palate and palm. Patient 9 hadpainful dysesthesia over the same area as patient 8 butadditionally had numbness in the first four toes. Patient11, who initially had mildly decreased position andvibration senses in the right arm and leg, soon showedsensory changes restricted to the fingertips.

Case 1. A hypertensive 52-year-old woman developedsudden numbness in the left arm and leg. On admission,her blood pressure was 160/110 mm Hg with regularpulse and no carotid bruits. Neurological examinationshowed normal motor function and reflexes. There wasa decreased sensation to pinprick, touch, vibration, andposition over the entire left side of her body. Graphes-

thesia and stereognosis were also impaired in the leftlimbs. Head CT performed 3 days after the onsetshowed an infarct in the posterolateral part of the rightthalamus (Figure 1). The hypesthesia and unpleasantnumbness continued.

Case 11. This 46-year-old hypertensive man suddenlyfelt heaviness in his right leg and complained of a gaitdifficulty. When he was first examined 2 days later hisblood pressure was 160/100 mm Hg, and he showedmildly decreased vibration and position senses in hisright arm and leg. The next day he complained ofnumbness restricted to the right distal fingers. Sensoryexamination showed impaired position sense in all rightfingers and decreased vibration sense restricted to thearea distal to the first interphalangeal joints. However,pinprick and touch senses were spared. Head CTshowed a small infarct in the left thalamus (Figure 2).

Lenticulocapsular or Corona Radiata StrokesFour patients (cases 12-15) with lenticulocapsular

strokes were identified. Patients 12 and 13 had lacunesin the lentiform nuclei abutting the posterior portion ofthe posterior limb of the internal capsule, and patients14 and 15 had very small hemorrhages near the middlethird of the posterior limb of the internal capsule. Threepatients showed very small (cases 16 and 18) or small(case 17) lacunes in the deep white matter of the middle

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Kim Pure Sensory Stroke 985

FIGURE 1. Computed tomography shows infarct in postero-lateral part of right thalamus.

cerebral artery territory, probably involving the coronaradiata. All of the patients with lenticulocapsular orcorona radiata stroke showed a decreased sense ofspinothalamic modality and suffered from a long-last-ing, unpleasant hemiparesthesia some time after theinitial events. Vibration and position senses were sparedin all of these patients. Patient 18 had suffered repeatedepisodes of sensory transient attacks.

Case 13. A 56-year-old hypertensive man awoke withnumbness in the left limbs. Neurological findings werenormal except for decreased pinprick and temperaturesenses over the entire left side of his body. His objectivesensory dysfunction gradually improved, but the un-pleasant hemiparesthesia continued. Initial brain CTwas negative, but a repeat scan performed 3 monthsafter the onset showed a small infarct in the rightlentiform nucleus abutting the posterior part of theposterior limb of the internal capsule (Figure 3).

Brain Stem StrokesTwo women with pontine strokes had PSS. One had a

small hemorrhage, and the other had an infarct in thetegmentum. Both showed an isolated sensory deficit ofthe medial lemniscal type.

Case 19. This 67-year-old hypertensive woman sud-denly felt numb in the left half of her body. In theemergency room her blood pressure was 230/140mm Hg. Cranial nerve and motor functions were nor-mal. Vibration and position senses in the left limbs weredecreased and were worse in the lower extremity.Pinprick and temperature were normally perceived.When standing, she veered to the left. Tl-weightedMRI performed 2 days after the onset demonstrated asmall hemorrhage in the right pontine tegmentum (Fig-ure 4).

Cerebral Cortical StrokesOne patient with cortical infarct showed PSS. Inter-

estingly, the PSS was preceded by multiple pure corticalsensory transient ischemic attacks.

FIGURE 2. Computed tomography shows small infarct inleft thalamus.

Case 21. A 65-year-old hyperglycemic and hyperlip-idemic woman developed intermittent abnormal sensa-tion and weak feelings in the left arm 7 days beforeadmission. These episodes occurred two or three timesa day and lasted usually less than an hour. During thoseattacks she could walk, but veered to the left, and theposture of her left arm became awkward. Neurologicalexamination showed a normal, obese woman, but duringthe attacks she showed a clumsy left hand with markedlydecreased vibration and position senses and abnormalstereognosis and graphesthesia. However, pinprick andtemperature senses were spared. A similar but lessmarked sensory abnormality was present in her left leg.

FIGURE 3. Computed tomography shows infarct in rightlentiform nucleus bordering posterior limb of internal capsule.

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986 Stroke Vol 23, No 7 July 1992

FIGURE 4. Tl-weighted magnetic resonance image (repeti-tion time/echo time, 600/20) shows high-signal intensity inright pontine tegmentum corresponding to location of mediallemniscus.

In addition, her left arm was observed to assume anabnormal posture: her elbow became gradually flexed to90° with her wrist and all fingers slightly flexed. She didnot notice this abnormal posture unless told, after whichshe could promptly correct it. During admission, therecurrent attacks led her to suffer PSS of corticalsensory deficit, which lasted about 5 days. Three daysafter admission T2-weighted and gadolinium-enhancedTl-weighted MRIs showed a small, linear, high-signalintensity in the cortical and subcortical areas of theright parietal lobe (Figure 5). An angiogram wasrefused.

DiscussionAs determined in previous investigations, the thala-

mus was the site most frequently involved in this series.Five patients showed an impairment of all sensorymodalities including pinprick, touch, vibration, and po-sition senses. Three patients had small infarcts (lacune)confined to the posterolateral part of the thalamus, andtwo had relatively large hemorrhages. Six patients withvery small lacunes showed restricted sensory changes:paresthesia without objective sensory signs (cases 6, 7,and 9), mild impairment in pinprick sense only (case10), and selective impairment in vibration and positionsenses (case 11).

Although thalamic strokes were usually reported toproduce deficits of all sensory modalities, Landi et al24

described a patient with decreased pinprick sense only,whereas Sacco et al27 reported a patient with a selectiveloss of the position sense. Therefore, small lacunesstrategically placed in the thalamus may cause tract-specific sensory deficits. According to previous studies,the medial lemniscal fibers are projected densely to thecaudal division of the ventral posterolateral nucleus,whereas the spinothalamic fibers diffusely enter theposterior thalamic nucleus, the ventral posterolateral

FIGURE 5. Gadolinium-enhanced Tl-weighted image (rep-etition time/echo time, 600/20) shows linear enhancing signal(arrows) in cortical and subcortical areas of right parietallobe. A clinically silent, old lacune is also seen in right basalganglia.

nucleus, and the central lateral nucleus.27 Presumablythe small lacune in patient 11 was situated within thecaudal part of the ventral posterolateral nucleus, butthis structure was spared in patients 6, 7, 9, and 10.

The patients with very small lacunes tended to showrestricted distribution of sensory abnormality, in thefaciobrachial area in patients 6 and 7 and the distalfingertips in patient 11. Patients 8 and 9 showed so-called "cheiro-oral syndrome": numbness restrictedover the corner of the mouth, hard palate, and hand.The present study and the previously reported thalamicstrokes with cheiro-oral sensory syndrome13-28"34 sup-port the alleged topographic presentation in the ventro-lateral nucleus of the thalamus34 in which sensory areasprojected from face and hands are closely related,although why the first four toes were also affected inpatient 9 remains unexplained.

There have been a few reports of PSS caused bycapsular or corona radiata strokes. Groothius et al17

suggested that to produce PSS, the lesion should occupythe posterior quarter of the posterior limb of theinternal capsule, where sensory tracts without motorfibers are believed to be located. In the present study,four patients with lenticulocapsular stroke with PSSwere identified: two (cases 12 and 13) had lacunesabutting the posterior quarter of the posterior limb, andtwo (cases 14 and 15) showed lesions bordering themiddle of the posterior limb, suggesting that smalllesions in this area could also escape the descendingmotor tract. Moreover, in this series three patients hadlacunes in the corona radiata of the middle cerebralartery distribution. A similar patient with a coronaradiata lacune in the middle cerebral artery territorywas previously reported by Rosenberg and Koller,23 andChamorro et al4 described a patient with PSS who hada CT-identified lacune in the anterior limb of theinternal capsule.

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Kim Pure Sensory Stroke 987

It is noticeable that all of the patients in the presentstudy with capsular or corona radiata stroke showeddecreased pinprick and touch senses without impairedvibration or position senses. The patient described byGroothius et al17 who showed an additional deficit in themedial lemniscal sensory modality had lesions in theposterior part of the posterior limb adjacent to thethalamus, whereas the patients in the present studyshowed lesions situated in the lateral part of the internalcapsule or corona radiata. Therefore, it may be postu-lated that the medial lemniscal sensory pathways runposteriorly and medially within the posterior limb of theinternal capsule, whereas those of spinothalamic modal-ities ascend more laterally and diffusely into the coronaradiata.

I observed two patients with brain stem stroke, onewith a lacune and another with a hemorrhage in thepontine tegmentum. Both revealed sensory deficits ofpure lemniscal modality caused by discrete lesionssituated in the medial lemniscus. A patient with similarclinical features was previously described by Graveleauet al,8 but patients with isolated spinothalamic modalityimpairment1015 or with only subjective sensory symp-toms5 have also been described. Therefore, strategicallylocated small brain stem strokes tend to produce sen-sory deficit of a single tract type. Recently, brain stemstrokes causing cheiro-oral sensory syndrome were alsodescribed.7*12-'4

Finally, I described a patient with cortical infarct whoshowed markedly impaired cortical sensation. Der-ouesne et al21 reported a similar case with a smallcortical infarct in the middle cerebral artery territory. Itis unique and of interest that patient 21 had purecortical sensory transient ischemic attacks. This pa-tient's abnormal posture during the sensory transientischemic attack was probably due to a loss of positionsense in the involved limbs.

In conclusion, the clinical-radiological correlation of21 cases in this study strongly supports the previousassumption that strokes anywhere in the sensory tractcan produce PSS. Sensory deficits of all modalities inone half of the body usually are associated with arelatively large lacune or hemorrhage in the area of theposterolateral thalamus, whereas tract-specific or re-stricted sensory abnormalities usually correlate with avery small lesion located in the sensory pathway.

AcknowledgmentI wish to thank Professor Onyou Hwang for her helpful

suggestions in preparing this manuscript.

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J S KimPure sensory stroke. Clinical-radiological correlates of 21 cases.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1992 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.23.7.983

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