© 1988 S. Karger AG, Basel 0014-3022/88/0281 -0051 $2.75/0 Eur. Neurol. 28: 51-56 (1988) Language and Memory Disturbances from Mesencephalothalamic Infarcts A Clinical and Computed Tomography Study C. Fensorea, L.G. Lazzarinob, A. Nappoa, A. Nicolaib 3 Divisione Neurologica Ospedale Civile, Viterbo; bDivisione Neurologica Ospedale Civile, Gorizia, Italia Key Words. Aphasia • Thalamic aphasia • Thalamic infarct Abstract. Three right-handed subjects presented impairment of consciousness, paralysis of vertical gaze, aphasia and memory disturbances. Computed tomography scans showed low-density lesions in the paramedian areas of the left thalamus. Neuropsychological examination revealed a fluent aphasia in one patient and a nonfluent in two; all had paraphasias and perseveration. Comprehension, repetition and writing were normal. In the literature on socalled thalamic aphasia only a few cases are reported with involvement of the paramedian nuclear complex. The mesencephalothalamic syndrome results from a circumscribed lesion - usually a lacunar infarct - involv­ ing the paramedian sites of the rostral midbrain, subthal­ amus and thalamus. The clinical features of the syn­ drome include consciousness and oculomotor distur­ bances [ 1-4], impairment of memory [1,5,6], motor and spatial neglect [1,5, 7], confusion [1,5, 8], and, in a few cases, aphasia [9, 10], Although the vascular anatomy of the thalamic region shows variations from subject to subject, usually the paramedian areas are supplied by the anterior thalamosubthalamic paramedian arteries [ 1, 11] (also termed thalamoperforating or deep interpeduncu­ lar profunda) that arise from the short trunk comprised between the basilar bifurcation and the origin of the pos­ terior communicating artery. Occasionally, a common penetrating branch from one side may supply both para­ median areas and this variation accounts for the simul­ taneous occurrence of bilateral infarcts that usually cause transient coma followed by neuro-ophthalmologic symptoms, drowsiness, amnesia, and dementia [1, 2, 5, 8, 12-19]. As few reports emphasize the association of neuroophthalmologic signs and aphasic symtpoms related to an involvement of the rostral midbrain and paramedian thalamic nuclear complex of the dominant hemisphere [9, 10, 19], we consider it useful to report three cases with the above-mentioned characteristics. Case Reports Case No. 1 A 67-ycar-old right-handed retired school teacher awoke from a brief afternoon nap with obtundation and inability to stand. An hour later, when he was admitted to the hospital, he appeared som­ nolent and passive; he could carry out only elementary instructions and responded with simple sentences which were scarcely intelligi­ ble due to paraphasic speech. The strenght of the limbs appeared normal; neither dysmetria nor sensory signs were seen. There was facial weakness in the lower right side. The pupils were of equal size, small (1.5 mm) and sluggish. In primary position there was slight left-eye hypotropia. Vertical gaze - in both directions - was impos­ sible either on pursuit or on saccades. Horizontal gaze (smooth pur­ suit and saccades) was impaired. Convergence was limited. The doll’s head maneuver resulted in ocular deviations which were impossible in voluntary efforts. An hour later, the patient was more somnolent and right hemiparesis appeared. Blood pressure was 150/80, pulse rate 80/min. Prednisone, glycerol and heparin were adminsitered. Twelve hours later the patient was alert, the right hemiparesis had cleared, but the gait was unsteady. The horizontal gaze was normal and the vertical unchanged, except for a limited (approximately 5°) downward gaze. Visual field was full on confron­ tation. Speech was fluent but with paraphasias, frequent semantic substitutions and occasional grammatical mistakes. Anterograde verbal memory was poor. A tendency to perseverate in questions Downloaded by: King's College London 137.73.144.138 - 1/13/2019 3:29:11 PM Introduction 52 Fensore/Lazzarino/Nappo/Nicolai and sentences was evident: no other neuropsychological distur­ bances were observed. An EEG recorded 36 h after the stroke showed bursts of theta and delta activity from the left parietal area. Eight days after admission, a computed tomography (CT) scan of the brain showed a small infarct in the medial thalamus of the left side. A repeated CT scan. 16 days after admission, showed a more hypodense lacunar lesion (Fig. I). Three weeks later, the difficulty in walking had disappeared; down gaze improved (approximately 15°). while upward gaze was unchanged. A complete neuropsychological examination (tables 1-111) was performed 3 weeks after admission when vigilance and attention disturbances could be ruled out (table I). A similar examination was repeated 6 months after the onset (tables I—III). Fig. 1. Case No. 1 CT scan without contrast ( 16th day) showing a pramedian nonhcmorrhagic infarction of the left thalamus in the territory of the paramedian thalamic arteries. Fig. 2. Case No. 2. Noncontrast CT scan (60th day) showing the ischemic lesion in the territory of the thalamic paramedian arteries involving the paramedian upper midbrain, subthalamus and (less extensively) the thalamus of the left side. Fig. 3. Case No. 3. Plain CT scan showing hypodense lesion involving the left thalamosubthalamic areas. Case No. 3 A 62-year-old right-handed woman was admitted to the hospital after being found comatose in bed. She had been well the previous evening and her past health was reported to be normal, apart from long-standing mild untreated hypertension. General examination was normal; blood pressure was 170/100, the pulse 72 regular, the respiration 19/min. Although stuporous, she was able to follow ele­ mentary verbal commands after vigorous stimulation and moaned in response to pinprick. Pupils were 4 mm and reactive bilaterally. At rest there was left exotropia; neither random eye movements nor pursuit could be observed, either in horizontal or vertical planes. Convergence could not be elicited; vertical oculocephalic move­ ments were normal, while the horizontal movements were full except for adduction of the left eye. A mild right hemiparesis was noted, with ipsilatcral extensor plantar response. Sensory functions were normal. An EEG on admission showed generalized slowing in theta and delta range. Over the next 4 days the level of conscious­ ness fluctuated. Vertical voluntary gaze still seemed completely absent, while vertical oculocephalic movements and Bell's phenom- Downloaded by: King's College London 137.73.144.138 - 1/13/2019 3:29:11 PM Case No. 2 A 44-ycar-old right-handed workman, suffering from rheuma­ toid arthritis, noted the sudden onset of horizontal diplopia fol­ lowed by speech disturbances. On admission he appeared apathetic and showed a complete left third nerve palsy. At rest there was a mild left exotropia. In the right eye there was a severe limitation (about 5°) of upward gaze, while the downward gaze was intact. Bell’s phenomenon was preserved and doll’s head maneuver in­ duced the upward gaze in the right eye. but no movement in the left one. Pupils were unequal in size (5 mm right: 2 mm left): both were sluggish to light. Motor examination showed a severe right hemiparcsis. Sensory functions appeared intact. The patient spoke in a whisper and nonfluent speech with profuse semantic paraphasias and tendency to echolalia. Visual field was normal on confrontation. Over the next few days there was remarkable improvement of con­ sciousness. while speech and memory disturbances were still present. An EEG recorded 24 h after admission showed diffuse theta and delta activity from the left hemisphere. Laboratory studies were normal apart from slight positivity of the RA test. Four days after admission a CT scan showed a low density in the rostral midbrain and medial side of the left thalamus. Sixty days later the CT scan (fig. 2) was virtually unchanged. He was discharged 2 months after the stroke: oculomotor disturbances were unmodified: right hemiparesis had improved. The first comprehensive neuropsychological examination was performed 4 weeks after admission and repeated 5 months after the onset (tables I-1II). 53 Thalamic Aphasia Table I. Examination of attention Patient No. 3 Patient No. 2 Patient No. 1 4 weeks 5 months 4 weeks 6 months Toulousc-Pierron’s barrage test (normal: 11 ± 6 min. *s 25 errors) 16 Time, min 36 24 Errors, n 30 37 43 20 30 40 45 25 30 Digit span (normal; 3= 5 forward, 5= 3.5 backward) Forward 4 Backward 3 5 4 3 4 5 3 3 3 5 3 Counting backward (20-1; normal: « 1 Is, no errors) Times, s 20 Errors, n 2 12 0 25 5 14 1 30 6 15 1 3 weeks 6 months Table II. Neuropsychological examination, according to Bisiach el al. [35] Spatial exploration Perception Apraxia Ideomotor Ideational Constructional For dressing Somatognosia and right-left identification Memory Digit span (0-7) Learning of paired words Easy pairs (7.5) Difficult pairs (15) Total (= 22.5) Recall of logical stories (normal: 12.6 ±4.3) Learning of 3 series of words (13.8 ±3.8) Visual memory (recall of configurations after 2 min) Memory for faces Autobiographic memory Reasoning Calculation (level of performance) Patient No. 1 Patient No. 2 Patient No. 3 3 weeks 6 months 4 weeks 5 months 4 weeks 6 months good good good good good good good good good good good good absent absent absent absent good absent absent absent absent good absent absent absent absent good absent absent absent absent good absent absent absent absent good absent absent absent absent good 4/7 5/7 3/7 4/7 3/7 4/7 4 7 11 6 9 15 3.5 6 9.5 5 7 12 3.5 5 8.5 5 6 11 7 8 5 7 5 5 6 9 5 8 5 6 good good good good low good good good good low good good good good low good good good good low good good good good low good good good good low enon were normal. A plain CT scan was performed 5 days after admission and showed a low-density area in the mesenccphalothalamic structures of the left side (fig. 3). During the next 2 weeks the slight right hemiparcsis had cleared; the patient remained apathetic and slept up to 14 h per day. When aroused she could execute and repeat simple orders. The spontaneous output was reduced and sev­ eral paraphasias and some perseveration were apparent. A formal neuropsychological examination was performed 4 weeks after the stroke, when she was sufficiently attentive (table II). On discharge the patient was alert, attentive and could walk. She had crossed diplopia to the right horizontal gaze; downward gaze was full, while upward had improved (approximately 15°). Troubles of speech and memory were still present. A fell reassessment was made 6 months later (tables I—III). Downloaded by: King's College London 137.73.144.138 - 1/13/2019 3:29:11 PM Test category Fensore/Lazzarino/Nappo/Nicolai 54 Table III. Results of Boston aphasia examination Test category Patient No. 1 Patient No. 2 Patient No. 3 4 weeks 6 months 3 5 2 4 6 4 4 3 100 100 100 100 85 70 80 80 80 75 90 90 85 90 80 95 100 100 100 80 96 90 96 100 100 96 90 100 90 80 80 80 80 90 90 100 100 90 80 100 100 90 80 90 90 3 8 3 3 10 4 ND ND ND ND ND ND 2 2 7 8 3 3 weeks 6 months 4 weeks 5 months 4 3 5 2 2 5 6 4 5 4 2 2 5 6 5 5 4 Auditory comprehension. % Word discrimination (72) Body part identification (80) Right-left discrimination (18) Commands (15) Complex material (12) 80 100 100 90 80 100 100 100 100 90 80 100 100 80 80 Naming, % Confrontation (105) Body part (30) 96 100 100 too 97 90 Reading comprehension, % Word picture match (10) Reading sentences and paragraphs (10) Writing Mechanics (0-3) Written confrontation naming Narrative writing (0-4) Fluency Overall severity (0-5) Articulatory agility (1-7) Phrase length (1-7) Grammatical form (1-7) Paraphasia (1-7) Repetition (105), % High-probability sentences (8) Low-probability sentences (8) 6 4 4 4 3 2 Methods High-resolution CT scan was performed on the three patients. Prediction of vascular area of the infarct was based on vascular supply as described by Castaigne et al. [1], Percheron [11] and Damasio [20]. Neuropsychological assessments were carried out at the following intervals after the onset: 3 weeks and 6 months in patient No. 1,4 weeks and 5 months in patient No. 2, 4 weeks and 6 months in patient No. 3, respectively. The examination was per­ formed with the patients sitting in front of the examiner. Each examination started with a careful assessment of the attention (ta­ ble I) which was tested by the Toulouse-Pierron barrage test and by some subtests of spatial exploration and perception (identification of superposed configurations, identification of colors). All patients were collaborative. Results of the attention test are reported in table I. At the moment of the first examination, attention was slightly impaired in all cases but not enough to interfere grossly with the language performances. The results improved on the second assessment and the residual disturbances (with respect to the verbal tasks, digit span, and counting backward) could be accounted for by the persisting verbal memory impairment. The right hemiparesis of patient No. 2 explained his poorer performances in the barrage test. Memory impairment and other neuropsychological deficits were evaluated according to the test series of Bisiach et al. [21], Apart from disturbances observed during the first days after onset, a mild verbal memory impairment was relatively stable over the following 4-6 months and appears to be part of the anterograde verbal mem­ ory deficiencies for all modalities (serial, associative, logical). On the other hand, anterograde visual, retrograde verbal and visual memory were well retained (table II). Language evaluation was performed according to the Boston Diagnostic Aphasia Examination (table 111): fluency subtest was rated according to the guidelines of Goodglass and Kaplan [22] and this rating was based on a sample of conversation speech and picture description tasks (cookie-thief). All the tests in which manual dex­ terity was necessary were performed by patient No. 2 with the left hand because of right hemiparesis. Downloaded by: King's College London 137.73.144.138 - 1/13/2019 3:29:11 PM ND = Not done. 55 Thalamic Aphasia The interest we find in the three case reports lies in the fact that the clinical picture was related to a small infarct in the medial thalamus-rostral midbrain and rests on the assumption that there were no concomitant lesions in cor­ tical areas (fig. 1-3). The possibility of a lesion smaller than the resolution capacity of the CT scanner is undeni­ able. However, it is unlikely that a small undetected cor­ tical lesion could produce the type and severity of symp­ toms observed, whereas its selectivity as well as the clin­ ical picture of a mesencephalothalamic syndrome coher­ ently indicate a lesion confined to the territory of the thalamic-subthalamic paramedian arteries [1,5, 11], Be­ cause of the common vascularization and anatomical con­ tiguity, medial lesions of the thalamus frequently involve the rostral midbrain causing paralysis of the eye move­ ments in the vertical plane. As ocular symptoms of this type have been frequently reported in the literature, even when they are produced by unilateral lesions [3,4, 14], the present paper omits to discuss the neuro-opthalmologic disorder and focuses on the peculiar language distur­ bances. Aphasia following unilateral thalamic lesion in the dominant hemisphere has been frequently described with hemorrhage [23-28], infarction [9, 10, 19, 29-32] and thalamectomy [33-36]. However, there is uncertainty concerning the role of dominant thalamus in generating language. A nonspecific participation has been proposed [37], On the other hand, assuming that the dominant thal­ amus might be involved in a complex feedback process used to monitor language formulation, some authors [22, 27, 38] consider thalamic aphasia as a transcortical dis­ turbance of language. Goodglass and Kaplan [22] speculate that the domi­ nant thalamus provides the control mechanisms exerted by the posterior centers of language on the verbal output. Cappa and Vignolo [27] consider the dominant thalamus involved in semantic aspects of the language and not in the phonemic ones. Other theories suggest that thalamic aphasia may reflect the role of the thalamus in arousal mechanisms [9, 30, 40]: these theories are currently known as ‘activation theories’. Luria [40], rejecting the idea that language changes with thalamic lesion represent true aphasia, pro­ posed the term of ‘quasi aphasia’. The pathology of thalamic lesions [23-26] does not help in defining the role of the medial nuclei in the lan­ guage because the lesions reported were hemorrhagic with the exception of the case of Davous et al. [10]- and it is reasonable to suppose that an infarction following a hemorrhagic event is unlikely to be selective. Experi­ ments with electrical stimulation [41, 42] and retrograde degeneration [43, 44] indicate that the pulvinar may be involved in language. These studies would confirm the clinical observations of Ciemins [24] and Mohr et al. [26], but are in contrast with the thalamectomy studies of Vilkki and Laitinen [36], Even though variabilities exist, the syndrome of tha­ lamic aphasia shows the following characteristics as the most common: (1) fluent but paraphasic language, (2) comprehension relatively well preserved, and (3) re­ petition minimally impaired or normal [38]. Aphasia from naturally occurring thalamic lesions per­ sists for weeks, months and even years, according to var­ ious reports [for this aspect refer to ref. 39]. Our case No. 1 conforms to the above-listed features, whereas the second and the third had nonfluent language. Even though less frequently reported, cases of nonfluent language after tha­ lamic lesions do exist [19, 27-30]. The possibility that a paramedian thalamic lesion of the dominant hemisphere could be responsible for language disorders is disputed in the literature: Lecours and Lhermitte [32], and GraffRadford et al. [5] deny it, while Michel et al. [19], and Davous et al. [10] found evidence of it. That the thalamus, along with other structures, is involved in memory functions has been described clini­ cally, both in unilateral and bilateral lesions [5, 8, 1319], and experimentally by stimulation of the left ventro­ lateral thalamus [45]. Our cases would confirm that a small paramedian lesion in the left thalamus can cause impairment of the verbal memory. Despite an extensive literature, language dysfunctions in left thalamic infarctions and their exact anatomical and neurophysiological bases remain speculative. Pre­ vious studies [10, 19] suggested that even the medial nuclear complex of the dominant hemisphere may play some role in language. Based on CT-clinical correlations, the cases we have examined seem to concur with these reports. References 1 Castaigne, P.; Lhermitte, F.; Buge A.; Escourolle, R.; Hauw, J.J.; Lyon-Caen, D.: Paramedian thalamic and midbrain infarcts: clinical and neuropathological study. Ann. Neurol. 10: 127-148 (1981). 2 Fisher, C.M.: Lacunar stroke and infarcts. A review. Neurology 32: 871-876 (1982). 3 Smith, M.S.; Laguna, J.F.: Upward gaze paralysis following uni­ lateral pretectal infarction: a computerized tomography correla­ tion. Archs Neurol. 38: 127-129 (1981). 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