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(Stroke. 1996;27:677-682.)
© 1996 American Heart Association, Inc.

Articles

Discriminative Sensory Dysfunction After Unilateral Stroke

Jong S. Kim, MD Smi Choi-Kwon, PhD, RN

From the Department of Neurology, University of Ulsan, Asan Medical Center, Seoul (J.S.K.), and the Department of Nursing, Dankook University, Cheon-An (S.C.-K.), South Korea.

Correspondence to Jong S. Kim, MD, Department of Neurology, Asan Medical Center, Song-Pa PO Box 145, Seoul 138-600, Korea.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose Although sensory deficits caused by stroke have been reported occasionally, dysfunction of discriminative sensation has seldom been studied in patients with unilateral stroke. The frequency and modality of bilaterally impaired discriminative sensation also remain to be clarified.

Methods With the use of specifically designed methods, we tested discriminative sensations including texture discrimination, two-point discrimination, stereognosis, point localization, and position sense in 67 patients with acute unilateral stroke. The locations of the lesions were identified with the use of CT and/or MRI. Thirty-two age- and sex-matched healthy subjects were used as a control.

Results Impaired discriminative sensation was common in patients with unilateral stroke (detected in 57 of the 67 patients) regardless of lesion location except for patients with lateral medullary infarction. Discriminative sensation remained intact in only 3 of 25 patients who were initially diagnosed as having pure motor stroke on the basis of conventional sensory tests. Point localization and stereognosis were bilaterally impaired in 17 of 39 patients and 7 of 38 patients, respectively, regardless of the laterality of the lesion. Dysfunction of other sensory modalities was observed exclusively on the side contralateral to the lesion.

Conclusions Discriminative sensory disturbances, which often occur bilaterally in some modalities, are common in patients with unilateral stroke even in those with intact sensory function on routine examination. The subtle disturbances of this sensation may explain, at least in part, the clumsiness of the patients that is not readily explained by conventional neurological tests.

Key Words: sensory stroke • sense • cerebrovascular disorders

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Recently, sensory deficits caused by stroke have been studied with clinical-radiological correlation.^{1 2} However, conventional sensory testing is often insufficient to precisely assess the amount of patients' sensory dysfunction. For instance, Samuelsson et al,³ after examining spinothalamic sensory dysfunction with the use of quantitative thermal testing, concluded that subclinical sensory impairment is prevalent in patients with lacunar infarction. Moreover, to our knowledge, thus far no studies have been conducted to elucidate the characteristics of discriminative sensory deficits in patients with stroke occurring in various locations. The frequency and modality of bilateral discriminative sensory deficit after a unilateral cerebral lesion are also unclear.

An understanding of discriminative sensory impairment is important because these subtle sensory disturbances might be related to the functional outcome of stroke patients.⁴ Therefore, in this study we attempted to evaluate the characteristics of sensory deficits with special reference to TD, PL, ST, 2-PD, and PS in patients with stroke occurring in various regions.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
We studied 67 consecutive patients with acute stroke (infarction or hemorrhage) who were admitted to Asan Medical Center between January and August 1995. The patients' ages ranged from 27 to 83 years (mean, 60 years). Exclusion criteria were as follows: (1) patients with transient ischemic attack; (2) patients with remaining neurological deficit due to previous strokes; (3) patients with a communication problem due to aphasia, decreased consciousness, severe dysarthria, or emotional disturbances; (4) patients with evidence of peripheral neuropathy by history and/or neurological examination; (5) patients evaluated more than 7 days after the onset of stroke; and (6) patients in whom imaging study (CT and/or MRI) was inconclusive in localizing the lesion. The control group included 32 age- and sex-matched subjects (17 men, 15 women; age range, 46 to 78 years [mean, 59 years]) who did not have a history of neurological disease and were normal on neurological examination.

Routine neurological examinations were performed including conventional sensory tests for pinprick, temperature, touch, and vibration. In addition, the following sensory tests were performed with the use of specific methods: TD, PS, ST, PL, and 2-PD of the fingers (thumb and third and fifth fingers). Pressure sensitivity was not examined since this was shown to be a poor indicator of sensory impairment compared with 2-PD and PL.⁵

For the TD test, the method developed by Carey et al⁶ was used with some modifications. Briefly, 13 metal molds with ridged surfaces were produced, and a plastic polymer was used for the final product. The finely graded plastic surfaces were marked by ridges at set spatial periods. The spatial periods of the 13 surfaces ranged from 1500 to 3000 µm (each spatial period of the surface increased by 50, 100, or 150 µm), with a constant ratio of ridge to groove. The patients were required to compare surfaces with various spatial periods with a 1500-µm control surface. Using a predetermined random sequence, subjects were required to indicate the rougher texture in six different sets; six plates were used, each housing six sets of textured surfaces of the entire range. Differences in the surface spatial periods were expressed as percent difference in the spatial periods, which ranged from 3.33 to 100 percent spatial increase [Percent Spatial Increase=(X-1500)/1500x100]. Responses were recorded as correct or incorrect for each set of surfaces. The TD threshold was determined to be the point at which the patients were 80% accurate in their responses.

The test device for PS was manufactured with the use of a semiconductor laser attached to the dorsal side of a hand and aligned to the third finger. A sheet was attached 30 cm from the wrist. Each position was quantitatively defined and marked on the sheet as 30 (cm) xtan , where was an angle between the baseline and the beam produced by a given position. Eight different wrist angles (-45°, -30°, -15°, 15°, 30°, 45° in flexion-extension and -15°, +15° in abduction-adduction) were tested in a predetermined random sequence. The difference between the chosen angle and that indicated by subjects was detected, and the average error over the eight positions was used as an index of proprioceptive discriminative deficit.

For the ST test, 12 objects (bottle cap, box, cotton, eraser, pencil, extension plug, key, screw, spoon, coin, safety pin, and watch) differing in size, shape, weight, and texture were placed in each hand, and the subjects were asked to name them.^{7 8 9} 2-PD was measured from the tips of the thumb and third and fifth fingers of each hand with the two-point esthesiometer known as the Disk-Criminator.^{5 7 8} The examiner performing the test asked them to say "one" if they felt it as one point and "two" if they felt it as two. The threshold for 2-PD was defined as the point at which 80% accuracy was achieved.

For PL, the method described in Corkin et al⁵ was used with a slight modification.¹⁰ A four-spoked pattern of dots was stamped on each palm. The distance between dots was 3 mm in each of the four 35-mm-long diagonals. The subjects were tested twice in succession with a blunt probe and instructed to say "same" if both stimuli were felt exactly at the same point and "different" if they were not.

The patients' deficits were graded as slight, moderate, or severe for each test. The lower limit was based on the performance of normal control subjects (Table 1). The upper limit for each test was determined by the maximum deficits (ST, 0; TD, 100 percent spatial increase; PL, 35 mm; 2-PD, >15 mm; PS, 26°) manifested by the patients. The deficit was considered slight when it was less than 34%, moderate when it was 34% to 66%, and severe when it was above 66% of maximum deficits. The data were analyzed with descriptive statistics, t tests, ², and ANOVA with the use of the SAS statistical package.

View this table: [in this window] [in a new window]   Table 1. Summary of Normative Data

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Table 1 summarizes the normative data obtained from both hands of 32 healthy subjects. There were no significant differences in data between right and left hands. The results of 2-PD of the fingers (thumb and third and fifth fingers) were averaged and represented as 2-PD of the hand since the values of 2-PD of each finger were not statistically different (F=1.26, P=.29).

We conducted the sensory tests within 1 week after the onset of stroke. The entire set of tests was repeated at least once within 3 days after the first examination. The results in each examination were identical in almost all patients, and in a few patients who showed slight differences we used the data obtained from the first test. All patients underwent brain CT (27 patients) and/or MRI (41 patients). The locations of the lesions were cortico-subcortical in 14 patients, lenticulocapsular in 24, thalamic or thalamocapsular in 15, and brain stem in 14.

We found that as many as 57 of the 67 patients had a discriminative sensory dysfunction of at least one modality. Furthermore, among 25 patients who were diagnosed as having pure motor stroke based on conventional sensory tests, only 3 had intact discriminative sensation. Bilateral deficit of sensation occurred in the modalities of PL (17 of 39 patients) and ST (7 of 38 patients) but not in other modalities. Two patients had mild deficit of PL in the side ipsilateral to the lesions. In patients with bilaterally impaired PL, 11 had right-sided lesions and 6 had left-sided lesions, whereas among 20 patients with unilateral impairment of PL, 9 had right-sided lesions and 11 had left-sided lesions. Bilateral impairment of ST was seen in 3 patients with right-sided lesions and 4 with left-sided lesions, while among 31 patients with unilateral impairment, 19 had right-sided lesions and 12 had left-sided lesions. The frequency of unilateral or bilateral impairment of PL or ST was not significantly different between right- and left-sided brain lesions (PL, ²=1.437, P=.213; ST, ²=0.649, P=.627).

Discriminative sensory deficits due to lesions at different locations are briefly described below, and the radiological location for cortico-subcortical stroke is presented in the Figure.

View larger version (30K): [in this window] [in a new window]   Figure 1. Lesion location of cortico-subcortical stroke. Black area indicates infarction; gray area, hemorrhage. Numbers indicate patients' numbers.

Cortico-Subcortical Stroke (Table 2, Figure)
Eleven patients had infarcts (left in 3, right in 8), and 3 had intracerebral hemorrhage (right in all 3). Thus, 11 had right-sided lesions. All patients except 2 showed discriminative sensory deficit of more than one modality: ST, TD, PL, and 2-PD were impaired in 10, 9, 6, and 6 patients, respectively. However, PS was impaired in only 4 patients. On conventional neurological tests, 3 patients were considered to have pure motor stroke, of whom 2 had a deficit in discriminative sensation. The deficit in TD and 2-PD always occurred in the side contralateral to the lesion, whereas impaired PL and ST were observed bilaterally in 3 of 6 and 2 of 10 patients, respectively.

Lenticulocapsular Stroke (Table 3)
Sixteen patients had infarcts (left in 9, right in 7), and 8 had hemorrhages (left in 5, right in 3). Impairment of ST, TD, PL, and 2-PD was observed in 13, 10, 15, and 6 patients, respectively. Bilateral impairment of PL and ST occurred in 6 of 15 and 3 of 13 patients, respectively. Other discriminative sensory deficits occurred only in the side contralateral to the lesion. Among 15 patients who had pure motor stroke by conventional sensory testing, 14 demonstrated discriminative sensory deficits. In some (patients 23, 25, 33, 34), the degree of deficit was moderate to severe.

View this table: [in this window] [in a new window]   Table 3. Sensory Impairment in Lenticulocapsular Stroke

Thalamic or Thalamocapsular Stroke (Table 4)
Nine had intracerebral hemorrhage (right in 6, left in 3), and 6 had infarcts (right in 2, left in 4). Thalamic strokes, particularly hemorrhagic strokes, generally caused severe sensory dysfunction on conventional testing, and the discriminative sensation deficit was also severe. None had intact discriminative sensation. Two with small hemorrhage, however, presented with pure motor stroke, in whom mild deficit of PL was noted. Impairment of PL, ST, TD, and 2-PD was detected in 13, 11, 9, and 10 patients, respectively. Seven patients had impaired PS. Bilateral impairment of PL and ST occurred in 4 of 13 and 2 of 11 patients, respectively.

View this table: [in this window] [in a new window]   Table 4. Sensory Impairment in Thalamic and Thalamocapsular Stroke

Brain Stem Stroke (Table 5)
All 14 patients had infarction: 2 in the midbrain (patients 54 and 55), 4 in the pons (patients 56 to 59), and 8 in the medulla (patients 60 to 67). One with midbrain infarction presented with bilateral ataxia, and 4 with pontine lesion had pure motor stroke, of whom discriminative sensory deficit was found in 3. Other patients had various sensory deficits on conventional testing. Three presenting with medial medullary syndrome had profoundly impaired sensation of lemniscal modality but also had mildly decreased pinprick sensation. In these patients, discriminative sensations were severely impaired. In contrast, all patients with lateral medullary syndrome had selective sensory impairment of the spinothalamic modality. In these patients, discriminative sensation remained intact except for one who had mildly impaired PL. Overall, bilateral deficit of PL was noted in 4 of 5 patients.

View this table: [in this window] [in a new window]   Table 5. Sensory Impairment in Brain Stem Stroke

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
In the present study we investigated the sensory dysfunction of 67 patients with acute stroke occurring in various parts of the brain, with particular attention to impaired discriminative sensations including TD, ST, PL, 2-PD, and PS. As a control group, we examined 32 age-matched healthy subjects. In accordance with previous reports,^{5 6 9 11} there were no significant differences in discriminative tactile sensory thresholds or object recognition scores between left and right hands in our control group. However, the threshold for PL was higher than that reported by Corkin et al,⁵ which could be explained by the much higher average age in our group.

In the human brain, the medulla oblongata is unique in that the tracts carrying sensations of the spinothalamic and lemniscal modalities are distinctly separated. With the recent advent of MRI, premortem localization of medullary stroke became possible,^{12 13 14 15} and our patients were clearly divided into those with lateral or medial medullary infarction. It was noteworthy that in our patients with medial medullary syndrome, in whom lemniscal sensory deficits were profound, the discriminative sensation was also markedly impaired. In contrast, almost all patients with lateral medullary syndrome had intact discriminative sensation despite definite sensory deficit of the spinothalamic modality. These results are in agreement with the theory that sensations involved in discrimination mainly travel through the medial lemniscal pathways.¹⁶

However, impaired discriminative sensation was not always correlated with positional sensory deficit. Generally, impairment of discriminative sensations such as ST, TD, and 2-PD was more prevalent than that of PS regardless of lesion location. This could result from the fact that the test for assessing PS may not be sensitive enough. Previous studies also reported intact PS despite evidence of the lemniscal sensory tract involvement.^{15 17 18 19 20 21} Stated another way, the lesions in the lemniscal tract in our patients with subcortical stroke might not have been severe enough to produce clinically evident positional sensory deficit.

Thus, our data demonstrate that a well-designed evaluation of TD, PL, and 2-PD can inform us of even minor dysfunction of discriminative sensations that cannot be assessed by conventional sensory tests. Furthermore, we found that as many as 22 patients who were initially diagnosed as having pure motor stroke actually had dysfunctional discriminative sensation. An understanding of these altered sensory functions is important since they may explain the subtle clumsiness or disability of patients who apparently have normal sensory functions. An experimental study using monkeys²² previously reported development of motor dysfunction after the section of the dorsal column, the sensory cortex, or both. It was speculated that various sensory inputs could change the excitability of cortical efferent zones before and during the execution of voluntary movements.

Whether the discriminative sensations are represented bilaterally in the human cortex remains a controversial issue. The presence of ipsilateral sensory disturbances has been repeatedly documented in experimental studies^{23 24} as well as in patients with unilateral brain damage.^{5 8 10 25 26 27 28} Carmon and Benton²⁵ previously reported that TD was occasionally impaired bilaterally after a unilateral brain lesion, which almost always occurred in patients with right-sided lesions. However, according to Corkin et al,²⁷ among 139 patients who underwent cortical excision, impairment of PL, PS, and 2-PD occurred bilaterally in 36%, 16%, and 4%, respectively. They also claimed that bilateral deficit of PL occurred with equal frequency in patients with left- or right-sided lesions.

In our study a bilateral deficit of TD was not found in any patients regardless of lesion location, which is at odds with the results of Carmon and Benton.²⁵ This discrepancy may have been caused by the different test methods used. Carmon and Benton²⁵ examined the tactile perception of direction, which is to some extent similar to the 2-PD or PL used in our study, which requires the appreciation of spatial relations. We found that impairment of PL but not 2-PD often occurred bilaterally. Whether the impairment of PL was bilateral or unilateral was not related to the laterality of the lesions. Therefore, our data generally agree with the results of Corkin et al.²⁷ However, although previous studies^{5 29} reported that astereognosis was essentially restricted to the contralateral hand of the patients with unilateral cerebral lesions, 7 of our patients had impaired ST bilaterally. One of them (patient 2), however, had a lesion in the left medial frontal cortex, which might have compressed the opposite hemisphere. The occasional bilateral deficit of discriminative sensation observed in our study appears to support the previous theory²³ that this sensation is not entirely mediated through the strictly crossing medial lemniscal tract but also through other bilaterally traveling pathways, including the anterolateral system.

Unfortunately, we were not able to present long-term follow-up data in this study. However, during the average admission period of approximately 10 days, the deficit of discriminative sensation generally did not improve, which is consistent with the previous report³⁰ that discriminative sensory deficits tend to be recovered late. Finally, although we tried to exclude the subjects with symptoms and signs of peripheral neuropathy, we did not perform a nerve conduction study in all patients. Therefore, subtle peripheral neuropathy may be attributed to bilaterally impaired discriminative sensation, particularly in patients with diabetes mellitus. However, this possibility appears unlikely, considering that patients with bilateral deficit of PL and ST did not have bilateral sensory changes in other modalities. Furthermore, the prevalence of bilateral sensory deficit was similar in patients with diabetes mellitus (4 of 12 patients) compared with those without (17 of 55 patients).

In conclusion, impaired discriminative sensations such as TD, PL, and 2-PD are frequently observed in patients with unilateral stroke occurring in various regions, even in those without an apparent sensory deficit on routine examination. These subtle sensory changes may contribute to the patients' neurological disabilities, often occurring bilaterally,⁸ that are not readily explained by conventional neurological examinations.

	Selected Abbreviations and Acronyms

 

2-PD = two-point discrimination PL = point localization PS = position sense ST = stereognosis TD = texture discrimination

View this table: [in this window] [in a new window]   Table 2. Sensory Impairment in Cortico-Subcortical Stroke

	Acknowledgments

 
This study was supported by the Nondirected Research Fund, Korea Research Foundation.

Received October 23, 1995; revision received December 18, 1995; accepted January 8, 1996.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Kim JS. Pure sensory stroke: clinical-radiological correlates of 21 cases. Stroke. 1992;23:983-987. [Abstract/Free Full Text]
2. Bassetti C, Bogousslavsky J, Regli F. Sensory syndromes in parietal stroke. Neurology. 1993;43:1942-1949. [Abstract/Free Full Text]
3. Samuelsson M, Samuelsson L, Lindell D. Sensory symptoms and signs and results of quantitative sensory thermal testing in patients with lacunar infarct syndromes. Stroke. 1994;25:2165-2170. [Abstract]
4. Rose L, Bakal DA, Fung TS, Farn P, Weaver LE. Tactile extinction and functional status after stroke: a preliminary investigation. Stroke. 1994;25:1973-1976. [Abstract]
5. Corkin S, Milner B, Rasmussen T. Somatosensory thresholds: contrasting effects of postcentral-gyrus and posterior parietal-lobe excisions. Arch Neurol. 1970;23:41-58. [Medline] [Order article via Infotrieve]
6. Carey LM, Matyas TA, Oke LE. Sensory loss in stroke patients: effective training of tactile and proprioceptive discrimination. Arch Phys Med Rehabil.. 1993;74:602-611. [Medline] [Order article via Infotrieve]
7. Dannenbaum RM, Jones LA. The assessment and treatment of patients who have sensory loss following cortical lesions. J Hand Ther. 1993;6:130-138. [Medline] [Order article via Infotrieve]
8. Jones RD, Donaldson IM, Parkin PJ. Impairment and recovery of ipsilateral sensory-motor function following unilateral cerebral infarction. Brain. 1989;112:113-132. [Abstract/Free Full Text]
9. Robertson SL, Jones LA. Tactile sensory impairments and prehensile function in subjects with left-hemisphere cerebral lesions. Arch Phys Med Rehabil. 1994;75:1108-1117. [Medline] [Order article via Infotrieve]
10. Semmes J, Weinstein S, Ghent L, Teuber H-L. Somatosensory Changes After Penetrating Brain Wounds in Man. Cambridge, Mass: Harvard University Press; 1960.
11. Louis DS, Greene TL, Jacobson KE, Rasmussen C, Kolowich P, Goldstein SA. Evaluation of normal values for stationary and moving two-point discrimination in the hand. J Hand Surg. 1984;9A:552-555.
12. Bogousslavsky J, Fox AJ, Barnett HJM, Hachinski VC, Vinitski S, Carey LS. Clinico-topographic correlation of small vertebrobasilar infarct using magnetic resonance imaging. Stroke. 1986;17:929-938. [Abstract/Free Full Text]
13. Sacco RL, Freddo L, Bello JA, Odel JG, Onesti ST, Mohr JP. Wallenberg's lateral medullary syndrome: clinical-magnetic resonance imaging correlations. Arch Neurol. 1993;50:609-614. [Abstract]
14. Kim JS, Lee JH, Suh DC, Lee MC. Spectrum of lateral medullary syndrome: correlation between clinical findings and magnetic resonance imaging in 33 subjects. Stroke. 1994;25:1405-1410. [Abstract]
15. Kim JS, Kim HG, Chung CS. Medial medullary syndrome: report of 18 new patients and a review of the literature. Stroke. 1995;26:1548-1552. [Abstract/Free Full Text]
16. Carpenter MB, Sutin J. Human Neuroanatomy. 8th ed. Baltimore, Md: Williams & Wilkins Co; 1983:643-705.
17. Meyer JS, Herndon RM. Bilateral infarction of the pyramidal tracts in man. Neurology. 1962;12:637-642.
18. Chokroverty S, Rubino FA, Haller C. Pure motor hemiparesis due to pyramidal infarction. Arch Neurol. 1975;32:647-648. [Abstract]
19. Leestma JE, Noronha A. Pure motor hemiplegia, medullary pyramidal lesion, and olivary hypertrophy. J Neurol Neurosurg Psychiatry. 1976;39:877-884. [Abstract]
20. Ho KL, Meyer KR. The medial medullary syndrome. Arch Neurol. 1981;38:385-387. [Abstract]
21. Paulson GW, Yates AJ, Paltan-Ortiz JD. Does infarction of the medullary pyramid lead to spasticity? Arch Neurol. 1986;43:93-95. [Abstract]
22. Asanuma H, Arissian K. Experiments on functional role of peripheral input to motor cortex during voluntary movements in the monkey. J Neurophysiol. 1984;52:212-227. [Abstract/Free Full Text]
23. Semmes J, Mishkin M. Somatosensory loss in monkeys after ipsilateral cortical ablation. J Neurophysiol. 1965;28:473-486. [Free Full Text]
24. Tasker RR, Organ LW, Hawrylyshyn P. Sensory organization of the thalamus. Appl Neurophysiol. 1976;39:139-153. [Medline] [Order article via Infotrieve]
25. Carmon A, Benton AL. Tactile perception of direction and number in patients with unilateral cerebral disease. Neurology. 1969;19:525-532. [Free Full Text]
26. Carmon A. Disturbances of tactile sensitivity in patients with unilateral cerebral lesions. Cortex. 1971;7:83-97. [Medline] [Order article via Infotrieve]
27. Corkin S, Milner B, Taylor L. Bilateral sensory loss after unilateral cerebral lesion in man. Trans Am Neurol Assoc. 1973;98:118-122. [Medline] [Order article via Infotrieve]
28. Vaughan HG, Costa LD. Performance of patients with lateralized cerebral lesions. J Nerv Ment Dis. 1962;134:237-241. [Medline] [Order article via Infotrieve]
29. Roland E. Astereognosis: tactile discrimination after localized hemispheric lesions in man. Arch Neurol. 1976;33:543-550. [Abstract]
30. Peele TL. The Neuroanatomic Basis for Clinical Neurology. 2nd ed. New York, NY: McGraw-Hill Publishing Co; 1965:443-469.

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, J. S. Articles by Choi-Kwon, S. Search for Related Content PubMed PubMed Citation Articles by Kim, J. S. Articles by Choi-Kwon, S.