= a ‘oan casittl Hemianesthesia, sensory neglect, and defective access to conscious experience G. Vallar, MD; G. Bottini, MD; R. Sterzi, MD; D. Passerini, MD; and M.L. Rusconi, MD Article abstract—We report a patient wit! han ischemic stroke in the vascular territory of the right middle cerebral artery who had left spatial neglect and left hemianesthesia. The patient showed a dissociation between defective verbal reporting of somatosensory stimuli delivered to the left hand and physiologic evidence from an autonomic index. This indicates that there was processing of undetected stimuli without the patient’s awareness, and suggests that the hemianesthesia was due, at least in part, to somesthetic hemi-inattention. NEUROLOGY 1991;41:650-652 Unilateral cerebral lesions may produce defects in bodily sensation in the contralateral half of the body. Although defective sensory processing is probably the most common cause of hemianesthesia,' hemi-inatten- tion may also produce contralateral hemianesthesia. It is difficult, however, to separate the attentional and the primary sensory components of the hemianesthesia.? Vallar et al® found that vestibular stimulation may tem- porarily ameliorate not only left spatial neglect,‘ but also left somatosensory deficits in right brain-damaged patients. This suggests that hemianesthesia may be a manifestation of hemi-inattention. We report a right brain-damaged patient who had left spatial neglect and left hemianesthesia. The patient showed a dissociation between defective verbal report of stimuli delivered to the left hand and physiologic evidence from electrodermal skin conductance re- sponses (SCRs). Case report. A 51-year-old man had sudden onset of left hemiparesis. When admitted to the hospital he was awake, alert, and cooperative. He showed a left hemiparesis, more severe in the left arm, with increased deep tendon reflexes, left homonymous hemianopia, and left hemianesthesia for touch, pinprick, and proprioception. When tested in his left hand with an adaptation of von Frey hairs,° he never responded to a hair of less than 1.00 mm in diameter, His EEG revealed right slowing. Doppler sonography showed distal occlusion of the right internal carotid artery. CT performed 25 days after stroke onset revealed an infarction in the vascular territory of the right middle cerebral artery involving the temporoparietal regions and extending to the frontal lobe (figure). SPECT ”=T'c-HM PAO showed hypoperfusion in the right temporo- parietal-occipital regions. The patient was aware of his neurologic deficits and did not show neglect for the left half of his body. He showed hemi- spatial neglect in line bisection and in a variety of cancellation tasks. For instance, in a letter-crossing test,® he failed to cross out 26 of 53 left-sided “H” target letters (49%), while in the right half of the sheet, omission errors were 5/51 (10%). Vestibular stimulation. The effects of vestibular stimula- tion on neglect and hemianesthesia were tested in the patient. The left external ear canal was irrigated with 20 cm® of ice water over 1 minute. In a line cancellation task before treat- ment, the patient crossed out 5/11 lines in the left half of the sheet; immediately after caloric stimulation his performance was errorless (11/11 lines), but 30 minutes later dropped to the baseline level (3/11 left-sided lines). Cancellation performance in the right half of the sheet was always errorless. The effects of caloric stimulation on hemianesthesia were tested by a 0.90 mm diameter hair. Stimuli were delivered to the right or the left hand in a random fixed order. Before each stimulus the examiner alerted the patient by saying “now.” Before treat- ment, the patient never responded to stimuli given to the left hand (0/40), whereas he was completely accurate for stimuli given to the right hand (40/40). After vestibular stimulation, however, he showed a significant improvement, being able to report 27/40 left-sided stimuli (x? = 40.75, df = 1, p < 0.001); 30 minutes later his accuracy in the detection of left-sided stimuli was again at the baseline level (0/40). Detection of right-sided stimuli, both after stimulation (40/40) and 30 minutes later (40/40), was perfect. In addition to the actual left- and right-sided stimuli, 20 catch trials, where the warning was not followed by a stimulus, were given in each session (before treatment, after caloric stimulation, and 30 minutes later) interspersed at random between the left- and right-sided stimuli. The patient was very accurate, making only one false alarm error. Electrodermal skin conductance responses to somatosen- sory stimuli. The observation that the patient's hemi- anesthesia could be temporarily ameliorated by vestibular stimulation suggested that attentional,” rather than pri- marily sensory, factors might play an important role in his somatosensory deficit. To assess whether physiologic pro- cesses of detection were present without overt and aware verbal report, we recorded electrodermal SCRs to somatosen- From the Istituto di Niguarda, Milan, Italy. Jinica Neurologica (Drs. Vallar, Bottini, Passerini, and Rusconi), Universita di Milano, and the Divisione di Neurologia (Dr, Sterzi), Ospedale Supported in part by a grant from the Consiglio Nazionale delle Ricerche to G. Vallar. Received August 14, 1990. Accepted for publication in final form October 24, 1990. Address correspondence and reprint requests to Dr. Giuseppe Vallar, Istituto di Clinica Neurologica, Universita di Milano, Via F, Sforza 95, 20122 Milano, Italy, 660 NEUROLOGY 41 May 1991 LL BS | | | Figure. CT showing an infarct in the vascular territory of the right middle cerebral artery. Table. Average latency (sec) and amplitude (uS) of SCRs and stimulus intensity (V) for reported and nonreported stimuli producing the responses in the patient and in two control subjects Patient Left hand Right hand Reported Nonreported Reported Nonreported (N=23/23) (N—13/24) (N=26/26) (N=3/21) SCRs Latency 217 212 2.01 2.33 (sec) (0.18) (0.49) (0.15) Amplitude 052 0.30 058 «= 0.18 (us) (0.27) (0.19) (0.20) Stimulus 191.3 175.0 10288 83.33, intensity (17.85) (10.21) (10.78) wv) Control 1 Control 2 Left hand Left hand Reported Nonreported Reported Nonreported (N=24/24) (N=1/23) (N=24/25) (N=2/22) SCRs Latency 2.20 2.40 214 2.40 (sec) (0.28) (0.33) Amplitude 0.25 0.10 0.65 0.26 (uS) (0.09) (0.36) ‘Stimulus 95.83 715 103.12 15.0 intensity (9.52) (10.97) ) N indicates the number of recorded SCRs out of the number of delivered stimuli. Values in parentheses are standard deviations. sory stimuli delivered to the left hand. (The patient was not diabetic and was free of polyneuropathy, which might have impaired the SCRs.) We used a DC amplifier with a balanced resistor bridge in the input, and a paper recorder. Ag-AgCl * — electrodes were placed on the palmar hypothenar surface of the unaffected right hand.’ The stimuli (0.5 msec duration) were delivered by a constant tension stimulator applied to the right or left index finger by means of a couple of stainless electrodes, We used an adaptive simple up-down procedure,* whereby the intensity level was decreased by a fixed amount | (25 V) if the patient verbally reported the stimulus, and in- a: | creased by the same fixed amount if the stimulus was not OS EY reported. A sequence of 50 stimuli was delivered to the left index finger of the patient. The initial three trials were used for practice and SCRs were not recorded. The stimulus level used in the first trial was well above threshold (initial value, 250 V). Control data using the same paradigm and apparatus were collected from two sources: (1) the patient himself, test- ing his unaffected right hand (initial value, 225 V) and (2) two right-handed age-matched normal subjects, in whom the stimuli were delivered to the left index finger. Results. The table shows latency and amplitude of SCRs, and intensity of the stimuli producing SCRs. In both the patient and the two controls, the average in- tensity for verbally reported stimuli was greater than for nonreported stimuli. In the patient, the reported and nonreported stimuli delivered to the unaffected right hand were, as expected, less intense than those to the left hand. Virtually all verbally reported stimuli pro- duced SCRs in both the patient (left and right hands) and the two matched controls. In the patient, 54% of the nonreported stimuli delivered to the left hand produced SCRs, compared with only 14% of the nonreported stimuli delivered to the right hand (y? = 7.77, df = 1,p < 0.005). The amplitude of the patient’s SCRs to ver- bally reported stimuli was greater than to nonreported stimuli (unpaired t test = 2.58, df = 34, p < 0.02), while no significant difference was found between SCR laten- cies (unpaired ¢ test = 0.48, df = 34, NS). Control subjects showed a pattern comparable to that observed in the patient’s unaffected right hand: SCRs to non- reported stimuli were rarely observed (4% in control 1 and 9% in control 2). The patient’s threshold in the unaffected right hand was comparable to that of the two controls: the mean intensity of all nonreported stimuli was 76.19 V (N = 21, SD 5.45) in the patient, 70.65 V (N = 23, SD 9.70) in control 1, and 75 V (N = 22, SD 0) in control 2. Discussion. Since more than 50% of the nonreported stimuli delivered to the patient’s left hand produced SCRs, an early phase of somatosensory processing stimuli was not entirely disrupted. The patient’s left May 1991 NEUROLOGY 41 651 ne ee ee hemianesthesia cannot, therefore, be attributed en- tirely to a primary sensory deficit. An important factor in producing the left hemianesthesia may be somes- thetic hemi-inattention.? The presence of autonomic responses in the absence of overt verbal reporting ar- gues that the patient’s hemianesthesia was due to defec- tive access of relatively preserved early analyses to the conscious processes required for verbal response. By contrast, in the patient’s unaffected right hand and in the left hand of the two control subjects, only a few SCRs to nonreported stimuli were recorded. Normal subjects may show SCR evidence of stimulus processing and discrimination in the absence of overt verbal iden- tification. Lazarus and McLeary® interpreted this as processing without awareness which, our data suggest, may underlie the somatosensory deficits of patients with spatial hemineglect. The present findings indicate that somesthetic hemi-inattention was an important factor in producing the patient’s left hemianesthesia. Meador et al,!° in 18 patients undergoing preoperative evaluation for epi- lepsy surgery, found that right intracarotid sodium amytal produces more severe somatosensory deficits (failure to detect single contralateral touches) and tac- tile extinction then left-sided injection. These data sug- gest both a hemispheric asymmetry in tactile attention, with a right hemispheric specialization, and the pos- sibility of an attentional component in the left hemi- anesthesia associated with right cerebral lesions. Our findings are confirmatory, and suggest that, in patients with spatial hemineglect, left hemianesthesia may be 662 NEUROLOGY 41 May 1991 ee a viewed as a component symptom of neglect. A basic — problem of the neglect syndrome may be the impaired — access to conscious mental activity by information that has undergone some unconscious analysis. This may be detected by physiologic measures. References 1. Adams RD, Victor M. Principles of neurology, 4th ed. New York: McGraw-Hill, 1989. Heilman KM, Watson RT, Valenstein E. Neglect and related disorders. In: Heilman KM, Valenstein E, eds. Clinical neuropsy- chology, 2nd ed. New York: Oxford University Press, 1985:243-293. Vallar G, Sterzi R, Bottini G, Cappa SF, Rusconi ML. Temporary remission of left hemianesthesia after vestibular stimulation: a sensory neglect phenomenon. Cortex 1990;26:123-131. |. Rubens AB. Caloric stimulation and unilateral visual neglect. Neurology 1985;35:1019-1024. Corkin S, Milner B. Somatosensory thresholds. Arch Neurol 1970;23:41-58. Diller L, Weinberg J. Hemi-inattention in rehabilitation. The evolution of a rational remediation program. In: Weinstein EA, Friedland RP, eds. Hemi-inattention and hemisphere specialization. Advances in neurology, vol 18. New York: Raven Press, 1977:63-82. . Fowles DC, Christie MJ, Edelberg R, Grings WW, Lykken DT, Venables PH. Publication recommendations for electrodermal measurements. Psychophysiology 1981;18:232-239. . Levitt H. Adaptive tests in audiology. In: Ludvingser C, Barfold J, eds. Sensorineural hearing impairment and hearing aids. Scand Audiol Suppl 1978;6:241-291. Lazarus RS, McCleary RA. Autonomic discrimination without awareness: a study of subception. Psychol Rey 1951;58:113-122. . Meador KJ, Loring DW, Lee GP, et al. Right cerebral specializa- tion for tactile attention as evidenced by intracarotid sodium amytal. Neurology 1988;38:1763-1766. 2 bad es a @ 1 S Neurology Hemianesthesia, sensory neglect, and defective access to conscious experience G. Vallar, G. Bottini, R. Sterzi, et al. Neurology 1991;41;650-652 DOI 10.1212/WNL.41.5.650 This information is current as of May 1, 1991 Neurology ® is the official journal of the American Academy of Neurology. Published continuously since 1951, it is now a weekly with 48 issues per year. Copyright . All rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X. AMERICAN ACADEMY OF NEUROLOGY. 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