COMMENT The results point toward a possible deleterious effect on memory of stan¬ dard anticholinergic therapy in par¬ kinsonian patients, reaching statisti¬ cal significance in one test of interme¬ diate memory and a similar trend in another. The digit span test for imme¬ diate memory was unaffected. Al¬ though the investigation was not dou¬ ble blind, the fact that medication apparently affected only some of the tests and not others may be taken to imply that observer bias was not cru¬ cial in evaluating results. The conten¬ tion that reduced cerebral levels of acetylcholine are associated with impaired memory function seems to be supported. Comparison with a group of normal age-matched subjects shows that par¬ kinsonian patients are at an initial disadvantage in intermediate memory capacity, although immediate capaci¬ ty is not impaired. This is of interest in view of the observation that in normal subjects physostigmine injec¬ tions enhanced performance in tests of long-term memory and retrieval while not affecting short-term re¬ sults.2 It has also been noted that the beneficial effects on memory of mea¬ sures presumed to increase cerebral acetylcholine levels, as well as the deleterious effects of administering anticholinergic drugs, are more marked in normal persons whose pre¬ treatment scores were relatively low." In light of their poor basic perfor¬ mance compared with that of normal subjects, it may be concluded that the anticholinergic drugs should be carefully considered in parkinsonian patients, especially those still engaged in occupations in which the function of memory is important. use of References 1. Drachman DA, Leavitt J: Human memory and the cholinergic system: A relationship to aging? Arch Neurol 1974;30:113-121. 2. Davis KL, Mohs RC, Tinklenberg JR, et al: Physostigmine: Improvement of long term memory processes in normal humans. Science 1978;201:272-274. 3. Drachman DA, Sahakian BJ: Memory and cognitive function in the elderly: A preliminary trial of physostigmine. Arch Neurol 1980;37:674\x=req-\ 675. 4. Sitaram N, Weingarten H, Gillin JC: Human serial learning: Enhancement with arecholine and choline and impairment with scopolamine. Science 1978;201:274-276. Aphasia After Right Thalamic Hemorrhage Howard S. Kirshner, MD, Kent H. Kistler, MD \s=b\ A 53-year-old hypertensive, con- verted left-handed man manifested aphasia after a right thalamic hemorrhage. The syndrome of mild, fluent aphasia, with naming difficulty and occasional paraphasic errors, but intact comprehension and repetition, is similar to that of previously reported patients with left thalamic lesions. The occurrence of aphasia after right thalamic hemorrhage suggests that right-hemisphere language dominance in left-handed subjects can extend even to the level of the thalamus. (Arch Neurol 1982;39:667-669) "increased attention has been di¬ rected in recent years to aphasie syndromes resulting from subcortical lesions, especially left thalamic hem¬ orrhage,17 left thalamotomy,8-'2 and most recently ischemie strokes in the vicinity of the left basal ganglia and internal capsule.1315 These lesions spare the perisylvian, frontotemporal language cortex, the traditional site of damage in aphasia. The involvement of left-hemisphere subcortical centers Accepted for publication April 16, 1982. From the Department of Neurology, Vanderbilt University School of Medicine, Nashville, Tenn, and the Nashville Veterans Administra- tion Medical Center. Reprint requests to Department of Neurology, Vanderbilt University School of Medicine, 354 Medical Center S, 2100 Pierce Ave, Nashville, TN 37212 (Dr Kirshner). in language processes has thus changed our understanding of the organization of language in the brain. We recently encountered a lefthanded patient with aphasia second¬ ary to spontaneous hemorrhage into the right thalamus. REPORT OF A CASE A 53-year-old, college-educated man was admitted to a local hospital after the abrupt onset of numbness and weakness of his left arm and leg. He had been in excellent health except for hypertension, with no medical history of stroke or tran¬ sient ischemie attacks. He wrote with his right hand but described being "converted" from left-handedness in childhood. At the local hospital, he was hypertensive (BP, 200/120 mm Hg), with a flaccid left hemi¬ paresis, somnolence, persistent headache, and nausea with frequent retching, requir¬ ing placement of a nasogastric tube. On transfer to the Nashville (Tenn) Vet¬ erans Administration Medical Center two days after onset, he was lethargic but arousable, spoke fluently with word-find¬ ing pauses and circumlocutions, and fol¬ lowed simple commands. He read sen¬ tences aloud, performed simple calcula¬ tions, copied geometrical figures, drew a clock, and showed no neglect of the left side. He had good insight and normal emotional expression. The cranial nerve examination disclosed only moderate weakness and decreased sensation of the left side of the face. There was no visual field defect to confrontation. He had a flaccid left hemiplegia, except for slight movement of the left toes, and a dense hemisensory loss to pin and touch involv¬ ing the left side of the face, extremities, and trunk to the midline. Vibration and position sense were nearly absent in the left arm and leg. Strength and sensation were normal on the right. The left plantar response was extensor, the right flexor. During the next two days, the patient became more alert and began to regain some use of his left extremities. A com¬ puted tomographic scan five days after onset (Figure) showed a large right thalamic hemorrhage. He was given dexa¬ methasone, and his condition continued to improve. Subsequent examinations dis¬ closed occasional paraphasic errors (eg, "belt" for "watchband") and persistent but improving difficulty in naming, of which the patient himself complained. Compre¬ hension and repetition were normal. There was no longer any drowsiness or psychomotor retardation. The left hemiparesis improved very gradually to the point of the patient's walking with assistance, but the profound left hemisensory deficit persisted largely unchanged to the time of discharge, six weeks after admission. The patient was evaluated with the Porch Index of Communicative Ability (PICA)16 and the Boston Diagnostic Apha¬ sia Examination (BDAE)17 17 and 28 days after onset, respectively. There was a mild, fluent aphasia, with intact auditory com¬ prehension and mild deficits in spontane¬ ous speech, naming, and writing. Perfor¬ mance on the PICA was at the 92nd percentile for aphasies with left-hemisphere lesions, with mean scores showing only mild deficits on all tasks except the writing Downloaded From: http://archneur.jamanetwork.com/ by a Karolinska Institutet University Library User on 05/24/2015 Computed tomographic scan of head shows large right thalamic hemorrhage. subtests. On the BDAE, occasional literal and paraphasic errors were recorded. Hes¬ itancy and delays were noted on the nam¬ ing subtests, but responsive naming, body part naming, and picture naming were nearly errorless. There was decreased flu¬ ency on animal naming (nine animals in 60 s; normal, 18). Subtests for fluency, audito¬ ry comprehension, repetition, oral reading, automatic speech, reading comprehension, and singing and rhythm all gave normal results or showed mild impairment, except for long latencies and occasional parapha¬ sic errors. Writing was mechanically defi¬ cient, but intact for spelling and grammat¬ ical constructions. COMMENT Aphasie syndromes with lesions involving the deep structures of the left hemisphere have been clearly established. Several reports27 have described a syndrome of fluent apha¬ sia with paraphasic errors, dysnomia, and preserved comprehension and repetition in patients with left tha¬ lamic hemorrhage. Mohr et al3 called attention to the fatigability of such patients; there is a rapid fluctuation between an alert state, with nearly normal language function, and an obtunded state, with marked para¬ phasias and perseveration. Luria18 suggested that the language disorder of left thalamic lesions may be more closely related to a "partial distur¬ bance of vigilance" involving verbal processes than to a true aphasia. Some authors1-3 have also suspected that thalamic hemorrhages may cause aphasia by pressure on adjacent structures such as the temporal isth¬ mus. A specific role of the thalamus in language function is suggested by the occurrence of aphasia in other left thalamic lesions including thalamic tumors,19 thalamotomy,812 and surgi¬ cal removal of a thalamic arteriove¬ nous malformation.18 Postmortem studies of thalamotomy patients have confirmed that even small lesions restricted to the left ventrolateral nucleus can be associated with mild but persistent aphasia." Disruption of short-term memory and object nam¬ ing have also been noted during elec¬ trical stimulation of the left pulvinar20 and ventrolateral nucleus.21 Some authors,2-4 indicating the known con¬ nections between the ventrolateral nucleus and the frontal cortex and between the pulvinar and posterior cortical areas, have suggested that thalamic lesions might produce apha¬ sia by disrupting the activation of cortical language centers. To the best of our knowledge, our patient is unique among reported cases of aphasia secondary to thalam¬ ic hemorrhage in that the lesion was in the right hemisphere. Alexander and LoVerme7 found no such cases either in their own experience or in their review of aphasia with intrace¬ rebral hemorrhages. Reported cases of aphasia after thalamotomy have also included either unilateral left or bilateral lesions, with the single exception of a left-handed woman described by Bell,10 in whom a proba¬ ble hemorrhage complicated a right cryogenic thalamotomy. This patient had severe aphasia, impairment of reading and writing, left hemiplegia, and visual inattention to the left. No evidence was presented to exclude damage to cortical structures. The right thalamic hemorrhage in our patient is analogous in size and location to the left thalamic hemor¬ rhages causing aphasia in dextrals.3·5·7 We presume that our patient was one of the minority of sinistrale who man¬ ifest language dominance in the right hemisphere.22 The hemorrhage could produce aphasia either by local dis¬ ruption of the thalamus or by pres¬ sure on the adjacent right temporal lobe. In the case of left thalamic hem¬ orrhage, as already reviewed, the presence of similar aphasias after surgical lesions812 affecting the thala¬ mus would suggest that direct damage to the thalamus is at least partially responsible for the aphasia. An addi¬ tional pressure effect on the right temporal isthmus, however, cannot be excluded. The occurrence of aphasia after right thalamic hemorrhage in our patient implies that language domi¬ nance in the right hemisphere of sinistrale may extend even to the tha¬ lamic level. The right-hemisphere lan¬ guage cortex in sinistrals could theo¬ retically make connections to subcor¬ tical centers by one of two routes: either directly to right-hemisphere subcortical centers, or indirectly, via the corpus callosum to the left-hemi¬ sphere language cortex, and then to left subcortical structures. The former pathway appeared to be opera¬ tive in our patient. Aphasia has not yet been reported with lesions of other right-hemisphere subcortical struc¬ tures, but only recently has attention been drawn to aphasia after ischemie infarction of the left caudate, puta¬ men, and internal capsule.13,5 Ross et al23 recently reported a case of infarc¬ tion of the right internal capsule with "motor aprosodia," or loss of the emo¬ tional tone of expressive speech. They concluded that, because the lesion lay below the level of corticocortical connections via the corpus callosum, the integration of left hemispheremediated propositional speech and right hemisphere-mediated affective Downloaded From: http://archneur.jamanetwork.com/ by a Karolinska Institutet University Library User on 05/24/2015 speech must occur at a subcortical, perhaps brain stem level. A better understanding of the importance of subcortical centers to the organization of language function in the brains of both sinistrale and dextrals awaits further study of patients with subcortical lesions. Investigation of those uncommon patients with subcortical infarcts or surgical lesions, rather than hemor¬ rhages, should help to clarify the rela¬ tive importance of local subcortical damage indirect pressure effects on the temporal lobes in producing apha¬ sie disturbances. This investigation was supported in part by Teacher Investigator Development Award 5K07NS00429-03 from the National Institute of Neurological and Communicative Disorders and Stroke to Dr Kirshner and by the Veterans Administration. Linda Meyer and Merrily Jones made available the BDAE and PICA test results. Jane S. Smith helped prepare the manuscript. References 1. Fisher CM: The pathological and clinical aspects of thalamic hemorrhage. Trans Am Neurol Assoc 1959;84:56-59. 2. Ciemins VA: Localized thalamic hemor- rhage: A cause of aphasia. Neurology 1970; 20:776-782. 3. Mohr JP, Watters WC, Duncan GW: Thalamic hemorrhage and aphasia. Brain Lang 1975;2:3-17. 4. Samarel A, Wright TL, Sergay S, et al: Thalamic hemorrhage with speech disorder. Trans Am Neurol Assoc 1976;101:283-285. 5. Reynolds AF, Turner PT, Harris AB, et al: Left thalamic hemorrhage with dysphasia: A report of five cases. Brain Lang 1979;7:62-73. 6. Cappa SF, Vignolo LA: 'Transcortical' features of aphasia following left thalamic hemorrhage. Cortex 1979;15:121-130. 7. Alexander MP, LoVerme SR: Aphasia after left hemispheric intracerebral hemorrhage. Neu- rology 1980;30:1193-1202. 8. Waltz JM, Riklan M, Stellar S, et al: Cryothalamectomy for Parkinson's disease. Neurology 1966;16:994-1003. 9. Selby G: Stereotactic surgery for the relief of Parkinson's disease: II. An analysis of the results in a series of 303 patients (413 operations). J Neurol Sci 1967;5:343-375. 10. Bell DS: Speech functions of the thalamus inferred from the effects of thalomotomy. Brain 1968;91:619-638. 11. Samra K, Riklan M, Levita E, et al: Lan- guage and speech correlates of anatomically ver- ified lesions in thalamic surgery for parkinsonism. J Speech Hear Res 1969;13:510-540. 12. Ojemann GA: Subcortical language mechanisms, in Whitaker H, Whitaker HA (eds): Studies in Neurolinguistics. New York, Academic Press Inc, 1975, vol 2, pp 103-138. 13. Barat M, Mazaux JM, Bioulac B, et al: Troubles du langage de type aphasique et l\l=e'\sions putamino-caud\l=e'\es.Rev Neurol 1981;5:343-356. 14. Naeser MA, Alexander MP, Helm-Estabrooks N, et al: Aphasia with predominantly subcortical lesion sites: Description of three capsular/putaminal aphasia syndromes. Arch Neu- rol 1982;39:2-14. 15. Damasio AR, Damasio H, Rizzo M, et al: Aphasia with nonhemorrhagic lesions in the basal ganglia and internal capsule. Arch Neurol 1982;39:15-20. 16. Porch B: Porch Index of Communicative Ability. Palo Alto, Calif, Consulting Psychologists Press, 1967. 17. Goodglass H, Kaplan E: The Assessment of Aphasia. Philadelphia, Lea & Febiger, 1972. 18. Luria AR: On quasi-aphasic speech disturbances in lesions of the deep structures of the brain. Brain Lang 1977;4:432-459. 19. Smythe GE, Stern K: Tumors of the thalamus: A clinicopathological study. Brain 1938; 61:339-360. 20. Ojemann GA, Fedio P, Van Buren JM: Anomia from pulvinar and subcortical parietal stimulation. Brain 1968;91:99-116. 21. Ojemann GA, Ward AA: Speech representation in ventrolateral thalamus. Brain 1971; 94:669-680. 22. Subirana A: Handedness and cerebral dominance, in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology. Amsterdam, North-Holland Publishing Co, 1969, vol 4, pp 248-272. 23. Ross ED, Harney JH, deLacoste-Utamsing C, et al: How the brain integrates affective and propositional language into a unified behavioral function: Hypothesis based on clinicoanatomic evidence. Arch Neurol 1981;38:745-748. Bent-Knee Pulling in the Diagnosis of Upper Lumbar Root Lesions Joe F. Jabre, MD, Ronald W. Bryan, MD \s=b\ The pain pattern of patients with upper lumbar root lesions can be elicited by a simple diagnostic test called bentknee pulling, in which the examiner pulls the half-prone patient's bent knee backward while putting forward pressure on the buttock. The technique was tested in seven patients with either clinically, myel- ographically, or electromyographically demonstrated L-3 and/or L-4 root lesions, and it successfully reproduced the pain in all seven patients. In all patients the result of straight-leg raising was negative. (Arch Neurol 1982;39:669-670) long recognized. Little attention has been given, however, to bedside tests for the diagnosis of L-2, L-3, and L-4 root lesions. Such tests have been described but have not gained wide acceptance and are infrequently men¬ tioned in discussions of upper lumbar root lesions. We discuss the reasons that these tests have not been more widely used, assess their specificity, and describe a technique that is easier to perform and that puts more stress on these roots. METHODS The patient lies half prone with his back to the examiner. Holding the leg by the foot, the examiner pulls the leg back with the knee flexed. With his other hand, he pushes forward on the patient's buttock, so that the hip is thrust anteriorly (Figure). Technique of bent-knee pulling: left, anterior view; right, posterior view. } he usefulness of the straight-legraising test for the bedside diagno¬ sis of L-5 and S-l root lesions has been Accepted for publication April 4, 1982. From the Department of Neurology, Louisiana State University School of Medicine, New Orleans. Reprint requests to 5640 Read Blvd, New Orle- ans, LA 70127 (Dr Jabre). Downloaded From: http://archneur.jamanetwork.com/ by a Karolinska Institutet University Library User on 05/24/2015