thalamic astasia: inability to stand after unilateral thalamic lesions

Thalamic Astasia: Inability to Stand afier Udateral Thalamic Lesions

Joseph C. Masdeu, MD,” and Philip B. Gorelick, MD

Inability to stand in the absence of motor weakness or marked sensory loss is usually considered to reflect midiine cerebellar disease. However, the 15 patients reported here had astasia related to unilateral thalarnic lesions, docu- mented by autopsy and computed tomography in 2 patients and by computed tomography in 13. The lesions, includ- ing infarction (6), hemorrhage (7), and tumor (2), involved primarily the superoposterolateral portion of the thalamus, but spared the rubral region. Alert, with normal or near-normal strength on isometric muscle testing and a variable degree of sensory loss, the patients could not stand and 7 of them could not sit up unassisted. They fell backwards or toward the side contralateral to the lesion. They appeared to have a deficit of overlearned motor activity of an axial and postural nature. In the vascular cases, the deficit improved in a few days or weeks. However, these patients had a tendency to sustain falls during the rehabilitation period.

Masdeu JC, Gorelick PB. Thalamic astasia: inability to stand after unilateral thalamic lesions. Ann Neurol 1988;23:596-603

Disturbances of sitting and standing balance are not generally discussed in the classical descriptions of the thalamic syndromes 11, 2) or in more recent publica- tions dealing with thalamic lesions {3-71. However, impairment of balance and ambulation has been noted following therapeutic thalamotomy [8, 91. Hassler 1 101 rematked that in the “first one or two weeks {after surgery] . . . the patients use the contralateral extremities rarely and awkwardly, so that they fall to this side.” Hypotonia or neglect has been postulated to underlie the transient tendency to fall {8-101. Falling cannot be ascribed to the presence of hemiplegia, because the limbs contralateral to the lesion are strong on isometric efforts. We describe a similar syndrome in 15 patients with unilateral thalamic lesions. Characteri- zation of this syndrome is important because the clinical picture may mimic cerebellar disease and the tendency to fall may complicate the rehabilitation period.

Patients and Methods Patients (from the Hines Veterans Administration, Michael Reese, Montefiore, or Bronx Municipal hospitals) with single unilateral thalamic lesions, who were unable to stand unsup- ported or had a marked tendency to fall despite mild or no weakness, were studied retrospectively. Each was examined by one of the authors during acute hospitalization. Patients with multiple lesions or on medications likely to induce ataxia were excluded. Brain lesions were identified by com-

puted tomography (CT) in all 15 patients. Autopsy results were available in 2 patients. The lesions were measured on CT or at autopsy and their relationship to anatomical land- marks was determined visually. Then the boundaries of each lesion were drawn manually on the corresponding thalamic sections of the atlas by Schaltenbrand and Wahren [ll) (levels 9.5, 4, and 1.5 mm to the intercommissural axial plane). Using a graphics program for an MC 68000 com- puter, the frequency distribution of involvement was plotted at those four thalamic levels for the 13 patients with vascular lesions (Fig 1).

Results Demographics and Pathological Findings Seven patients had thalamic hemorrhages, 6 had infarcts, and 2 had glioblastoma multiforme, 1 proven by autopsy and the other by biopsy (Table 1). The average age of the patients with vascular disease was 69 years (range, 55-79). There were 10 men and 5 women. Hypertension was present in 11 patients, and 3 had diabetes. Patient 6 had polycythemia Vera. Eleven patients were on medications that included antihyperten- sives, diuretics, or cardiac drugs. None were on psy- chotropic agents or sedative-hypnotic drugs.

Neurological Findings Patients 1 and 7 had transient impairment of alertness in the second day of their hospital stay. Language defi-

From the Department of Neurology, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, NY, and the Depart- ment of Neurology, Michael Reese Hospital, The University of Chicago Prinker School of Medicine, Chicago, IL. Received Oct 1, 1987, and in revised form Dec 17. Accepted for publication Dec 30, 1987.

Address correspondence to Dr Masdeu, Department of Neurology, St Vincent’s Hospital and Medical Center, 153 West 11 th Street, New York, NY 10011.

*Current address: Department of Neurology, St Vincent’s Hospital and Medical Center of New Ydrk (New York Medical College), and the New York University Medical School, New York, NY.

596 Copyright 0 1988 by the American Neurological Association

ISuDero-Lateral 1

Frequency distribution of involvement:

IJ I case 4 cases 7 cases

0 2 cases 5 cases 8 cases 0 3 cases 13 6 cases 9 or more

Fig I . Diagram of horizontal sections of the thalamus shozuing the regional frequency distribution of lesions. For the sake of simplij5cation both right- and left-side lesions have been plotted on kjit thalamic sections, viewed from their medial aspect and top. The sections, modzj5ed from the atlas by Schaltenbrand and Wahren 51 I}, correspond to levels 9.5, 4, and 1.5 mm to the intercommissural axial plane. Heavier shading indicates a greater number of cases where that region was involved. The code is at the bottom of the &re. A = anterior nuclear group; CM = centromdial nudeus; DM = dorsomdial nucleus; GP = globus pallidus; Pf = parafascicular nucleus; Pt = putamen; Pu = pulvinar; VA = ventralanterior nucleus; VL = uen- trolateral nucleus; VP = ventral posterior nucleus.

cits consisting of impaired comprehension or fluency but preserved ability to repeat were observed in 4 of the 5 patients with left thalamic lesions. The remaining patient had a small infarct involving the superior portion of the left ventrolateral thalamic nucleus and suprathalamic white matter. Memory was affected in 2 patients. Four had visual field defects and 3 had impaired pursuit eye movements toward the side of the lesion.

Leg strength on volition was normal in 4 patients

Table 1. Demographics and Lesion Localization

Patient Age Thalamus Thalamic Region No. Sex (yr) Involved Involved

Hemorrhages 1 2 3 4 5 6 7

Infarcts 8

9 10

11

M 55 Rght M 56 Left F 63 Right M 66 Rght M 68 Left M 74 Rght M 76 Left

M 65 Left

M 72 Left F 73 Right

M 74 Rght

12 F 7 9 Right 13 F 79 Right

Tumors 14 F 57 Right 15 M 64 Rght

Dorsal Dorsoposterolateral Dorsal Dorsal Lateral Dorsal, pulvinar Anterior, dorsomedial

Suprathalamic white

Only anteromedial spared Ventrolateral, deep

Ventrolateral, ventro-

matter

parietal

posterior, suprathalamic white matter

Ventrolateral Ventroposterolateral,

internal capsule

Anterolateral Ventrobasal

and slightly impaired in the remaining 11 patients (Table 2). On a 1 to 5 scale 1121, all had motor power of 4 or better. The tone in the limbs contralateral to the lesion was slightly increased in 2 patients, moderately increased in 1, decreased in 1, and normal in the remaining 1 1 patients. Reflexes were contralaterally brisk in 5 patients and symmetrical in the rest. Babin- ski's sign was present in 8 patients and 6 had decomposition of distal movements, with an athetoid quality, but no terminal tremor. Unilateral asterixis was noted in 4 patients. Hemiballismus, chorea, or tremor was not present. Sensation was normal in 2 patients, sub- jectively altered in 2, mildly impaired in 6, moderately impaired in 4, and severely impaired in 1.

htasia Characteristics The onset of inability to stand unattended was sudden in all of the patients with vascular disease except 3 who had infarcts and deterioration of balance within a period of hours to 3 days. Eight of the patients could not even sit up by themselves and had marked truncal instability, falling backward or to the affected side from a sitting position when left without support. Typically, when asked to sit up, rather than using the axial muscles, these patients would grasp the side rail of the bed with the unaffected hand or with both hands to pull themselves up.

When lying supine and asked to push themselves up in bed, the patients would fail to use the limbs contralateral to the lesion, giving the impression of being hemiplegic. However, they would use the limbs on command, showing normal strength or only mild weakness for voluntary isometric efforts such as keep-

Masdeu and Gorelick Thalamic Astasia 597

Table 2. Neurological Findings

Strength".b

Sensory LOSS^^ Inability Inability Arm k Patient to Stand to Sit No. (days) (days) Proximal Distal Proximal Distal Tonea' Reflexes".' Babinski's Pin

Hemorrhages

Position Vibration

1 21 7 4.5 4.5 4.5 4.5 + N + + + + 0 2 35 12 4 4.5 4 4.5 N + + + + + + + +

20 12 4.5 4 5 5 N N 0 0 0 0 4 32 5 4.5 4.5 4.5 4.5 + N 0 + + 0 3

6 30 6 4 4.5 4 4 N N + + + + + + 5

7 10 5 4.5 5 4.5 4.5 + + + + 0 0 0

4 3 4.5 4.5 5 5 N + + + + + + + + + + +

Infarcts 8 1 0 5 5 5 4.5 N + + + + 0

10' 0 5 5 4.5 5 N N + + + 0 10 6 0 5 5 5 5 N N 0 0 0 0 9

11 4 1 4.5 4.5 4.5 4.5 + N 0 + + + + 12 1 0 4.5 5 4 4.5 N N 0 + 0 0 13 6 0 4 4 4.5 4.5 N N 0 + 0 0

14' 0 4.5 5 5 5 N N 0 0 0 0 15' 0 4 4 4 4 N + + + + +

Tumors

"Findings on the side of the body contralateral to the thalamic lesion. bNormal = 5; no trace of movement = 0. ' N o d (N); minimally (+) to markedly (+ + +) increased. dMinimal (+) to severe (+ + +) sensory loss. 'Patient died on the tenth day after ictus. 'The inability to stand was progressive in these patients with tumors. 0 = absent.

ing the elbow or the wrist extended. In some instances, the power of wrist extension would fluctuate within a matter of seconds as athetoid dystonia blended with voluntary effort.

In several patients, upon standing the affected knee was slightly flexed and the foot inverted. Balance transiently improved when the patient voluntarily cor- rected the position of the leg, but not enough to enable independent station. Poor activation of the proximal muscles as compared with the distal ones was observed in 5 patients and recorded in 3 by surface electrodes. This finding was more pronounced with overlearned associated movements. When eating, these patients could handle the fork deftly, using the fingers and wrist; the shoulder, however, was kept ad- ducted, with the elbow fixed against the chest, failing to support the forearm for the normal circling movement involved in lifting food from a plate. By contrast, they were able to abduct the shoulder on command, often with full strength.

Five patients could not carry out a repetitive motor task simultaneously with both hands or feet (asymul- tergia). For instance, they could repetitively tap the floor with the affected foot, but when asked to per- form the same tapping movement with both feet, the affected foot remained motionless.

Inability to sit unassisted lasted for an average of 7 days in the group of patients with thalamic hemorrhage, whereas only 1 of the patients with infarction

had transient difficulty sitting up. The inability to stand unassisted lasted for an average of 2 1 days in the group of patients with thalamic hemorrhage and for an average of 3 days in the group of patients with infarction. During recovery the patients were usually aware of their poor balance and some were fearful that they would fall when attempting to walk. Nonetheless they were not always able to prevent falls. Patient 7 fell and broke his hip 32 days after stroke onset.

Illustrative Case Reports PATIENT 3. A 63-year-old hypertensive woman fell down while in the bathroom. There was no loss of consciousness or hemiparesis but she was unable to stand. CT disclosed a right thalamic hemorrhage, centered in the superior portion of ventrolateral thalamic nucleus and in the suprathalamic white matter (Fig 2). She was alert and fully oriented. Language and memory were normal. Visual fields were full. Pursuit eye movements to the left were impaired. When asked to raise her arms, the patient lifted only the right one, but when directed ta move the left side, her strength was almost normal in both the left arm and leg. Mild rigid- ity was present on the left. Reflexes were symmetrical and plantar responses were flexor. Finger-to-nose and heel-to-shin maneuvers were performed slowly and clumsily on the left side. Sensory examination was normal. She could not bring herself to a sitting position for 12 days after admission. When attempting to sit up,

598 Annals of Neurology Vol 23 No 6 June 1988

Fig 2. Patient 3 . Computed tomograph shuwing a right thakzmic hemowhage, centered in the superior portion of the ven- tmkzteral nucleus and the suprathakarnic white matter.

she held the side rail with her unaffected hand only and tried to pull herself up. Upon further instigation by the examiner, she held the side rail with both hands and tried to pull herself up, but not using the trunk or leg muscles. When helped to the sitting position, she had marked truncal instability. She was unable to stand by herself for 20 days after the stroke. When assisted to the standing position, she fell backward or to the left. Two months later she could walk with supervision on parallel bars. When standing, the left knee tended to jerk into flexion and the ankle inverted minimally. Prompted to straighten out the left leg, she could then place weight on that leg and proceed to advance the right leg. Four months after the stroke she walked with a rolling walker, but her station remained impaired.

PATIENT 7. A 76-year-old, right-handed retired public accountant had diabetes mellitus controlled with oral hypoglycemic medication. On the day of admission he collapsed on the floor but remained alert. In the emer- gency room he was noted to be disoriented to time and place. He could not stand or sit up unassisted despite normal motor power. Because of the lack of a motor or sensory deficit the initial diagnostic impression was hypoglycemia. Normal blood chemistries prompted CT, which slowed a left thalamic hemorrhage, centered in the superior portion of the ventrolateral thalamic and ventral anterior nuclei. The lesion extended into the dorsomedial nucleus and the suprathalamic white matter (Fig 3).

Alertness was transiently impaired on the second hospital day. On the fourth hospital day, Boston Di- agnostic Aphasia Examination 1133 and the Boston Naming Test El41 delineated an aphasic syndrome

characterized by grammatically correct but complex, disorganized, and uninformative spontaneous speech and writing; frequent perseverations; and occasional phonemic paraphasias. With repetition of low-prob- ability sentences there were phonemic literal substitu- tions and spoonerisms. Comprehension of complex material was mildly impaired. Visuospatial and con- structional abilities and faciobuccal praxis were normal. On the Mattis Dementia Rating Scale El51, performance was poor on the subtests for initiation and perseveration (38%) and for memory (40%).

Emotional expression was diminished on the right side of the face. He perceived thermal, positional, and vibratory stimuli equally on both sides of the body. There was no extinction on double simultaneous stimulation. When asked to resist the examiner with his right extremities, the patient displayed an almost normal strength. However, he did not use the right limbs in the context of associated movements, such as when attempting to sit up, which he could not do for the first 5 days without help from an attendant. On command, he deftly held a spoon with his right hand and moved it in all the requested directions. However, after an attempt to bring food into his mouth from a cup of jello on his tray had failed because of the lack of associated proximal movements of the right arm, he picked up the cup with his left hand and brought it close to his mouth, pushing the food clumsily into his mouth rather than using his right hand. A mild flexion spasticity was present in the right arm, but not in the leg, and there was a right Babinski's sign.

He could ambulate with a walker on the tenth hospital day. He was transferred to a rehabilitation facility and his gait improved, but on the thirty-second hospital day he fell, fracturing his right femur. Twenty-five days later he suffered a myocardial infarction and died. Autopsy was not obtained.

Masdeu and Gorelick: Thalamic Astasia 5 9 9

~

Fig 3. Patient 7. Computed tomograph showing a left thalamic hemorrhage, centered in the superior portion of the ventrolateral thakzmzc and the ventral anterior nuclei and extending into the dorsomedial nucleus and the suprathalamic white matter.

PATIENT 9. This 72-year-old carpenter noted progressive difficulty ambulating over a 3-day period, to the point where he was unable to walk unassisted. His speech was characterized by circumlocutions and word-finding difficulties, but he was fully oriented. Vi- sual fields were normal. Despite good strength of both upper and lower extremities, the patient was unable to stand by himself and fell to the right side or backward. When asked ro raise the right arm, he could lift it up and maintain it in an abducted posture, but the arm drifted down when the patient was distracted. Muscle stretch reflexes were symmetrical. Tone in the right leg was slightly diminished. A right Babinski’s sign was present. There was a slight decomposition of movement on finger-to-nose and heel-to-shin testing. Pin- prick perception was intact. Vibratory and position sense were mildly impaired in the right leg. CT showed an area of hypodensity in the left thalamic region.

On the tenth hospital day the patient suffered mas- sive hematemesis and died. Necropsy of the brain re- vealed a left thalamic infarct with multiple petechial hemorrhages. The lesion was centered in the ventrolateral nucleus and involved most of the thalamic nuclei, except the anterior nuclear group (Fig 4). A small parathalamic area in the posterior part of the posterior limb of the internal capsule showed ischemic changes, with vacuolization of myelin sheaths and clusters of swollen axons. The brainstem and cerebellum were normal.

Discussion The term astasia is derived from the Greek negative particle a and the word stusis, meaning “station.” Dor- land’s IIIastrated Medical Dictionary 1161 defines astasia as “motor incoordination with inability to stand.” It

Fig 4 . Patient 9. Horizontal section of the brain through the thalamus showing a left thalamic infarct involving the lateropos- terior nuclear region. For more details see Case Report.

seems appropriate to apply this term to the syndrome displayed by our patients. The disturbance differed from cerebellar ataxia in that gait was not broad-based or lurching. It resembled, however, the marked balance impairment of patients with vestibulocerebellar disease. It may be argued that the term astasia should not be used in the context of organic brain disease, because it has customarily been applied to psychogenic gait impairment. As DeJong {17] remarks, “the term


astdsia-abasza has been given to the type of gait disturbance which is sometimes observed in hysterical indi- viduals. These words, however, actually mean ‘inability to stand and walk,’ and it is better to use the term hysterical dysbasia . . . ” when referring to psychogenic disturbances of gait.

Inability to stand or walk despite minimal weakness has been recorded with thalamic infarction [18, 191 and hemorrhage 120, 21). It has also been reported in patients with lesions in the internal capsule or corona radiata who had the syndrome of unilateral ataxia and crural paresis (ataxic hemiparesis) 122-251. Inability to walk despite good strength was also recorded by Groothuis and associates 1261 in a patient with a small medial capsular hemorrhage involving the most lateral portion of the ventrolateral nucleus of the thalamus. Our patients’ lesions were clustered mainly in the superior portion of the ventrolateral nucleus of the thalamus, and in some the suprathalamic white matter was affected (see Fig 1). Although good correlation of anatomical and CT findings has been reported in the case of ischemic lesions of the thalamus 1271, care must be exercised when drawing anatomical conclu- sions from CT data. Infarcts may appear smaller, even in the chronic stage and on high-resolution CT 1281. Recent hemorrhages are accurately depicted by CT; however, mass effect and edema surrounding the lesion cause dysfunction of apparently uninvolved structures. These factors pose less of a problem when the hemorrhages are small, such as those in our patients.

The ventrolateral nucleus of the thalamus consists of two portions 129, 30). The smaller anterior portion receives projections from the medial globus pallidus via the thalamic fasciculus and projects to area 6 of the frontal cortex. The larger posterior portion receives cerebellar, spinothalamic, and vestibular afferents and projects in a somatotopic fashion to area 4 of the precentral gyrus 1291. Medial neurons project to the lateral part of the precentral gym, whereas latero- superior ones project to the medial portion of the precentral gyrus, where the trunk and leg are represented. Fibers destined for the leg region course in the posterior limb of the internal capsule and then ascend in the more medial portion of the corona radiata, near the wall of the lateral ventricle. These fibers were probably involved in previously reported capsular cases of ataxic hemiparesis [22-251. Impairment of gait in the elderly with periventricular white matter disease might be related to involvement of this pathway { 3 11. Through the fastigial projection, the posterior portion of the ventrolateral nucleus of the thalamus receives informa- tion from the vestibulocerebellum {32). Bilateral rep- resentation of this projection, affected in our patients at the level of the thalamus, may be one of the factors explaining the transient nature of thalamic astasia.

Incoordination of movements resembling cerebellar

dysmetria has been reported with thalamic lesions [2 1, 331. Lesions of the inferior portion of the thalamus and red nucleus have been associated with marked inten- tion tremor (“rubral tremor”) 16, 34, 351. None of our patients had tremor. Clumsiness of distal movements was reminiscent of cerebellar dysmetria. However, in 7 patients athetoid posturing contributed to the inexac- titude and clumsiness of the distal movements. In addi- tion, the movement often became more accurate as the target was approached, unlike the pattern of movement known as cerebellar terminal dysmetria.

The syndrome described here differs from pyrami- dal weakness due to corticospinal tract damage, which when mild to moderate is generally accompanied by distal weakness but enough extensor tone of the lower extremity to allow safe station and ambulation 1361. In our patients and others with thalamic lesions the proximal muscles were weaker 15, 21, 371. With corticospinal tract damage, voluntary movements tend to be most affected 136, 381. In contrast, on command our patients used limbs that seemed paralyzed when per- forming actions that required automatic synergistic movements, such as pushing themselves up in bed.

Thalamic akinesia has been reported in patients with right thalamic [lS, 19, 39, 401 or left thalamic {9, 371 lesions. This deficit of motor control differs from non- dominant parietal neglect, which manifests as hemi- spatial neglect, anosognosia, tactile allesthesia, topo- graphic disorientation, and hemiasomatognosia, and which is often present to a mild degree in patients with right thalamic lesions 13, 18, 24, 41, 421. Similarly, a language disturbance is present in those with left thalamic lesions 120, 41, 431. Lateralizing manifestations of thalamic disease reflect the diverse specializa- tion of the cortex and subcortical structures targeted by fibers originating in the thalami or coursing through them. These lateralizing findings confound the analysis and interpretation of the akinesia associated with thalamic astasia, a finding that is probably common to lesions of either thalamic nuclear complex.

Thalamic akinesia may be partially related to damage of pallidothalamic and thalamostriatal connections. Bi- lateral pallidal damage causes akinesia 1441. Damasio and associates 1451 reported a patient (Patient 5) with akinesia of the arm contralateral to a striatal infarct. Some of the clinical findings in our patients mimicked deficits resulting from basal ganglia disease, namely proximal hypokinesia, poverty in the performance of automatic associated movements, and impairment in postural reflexes. They also share with parkinsonian patients the tendency for flexor posture of the legs, noted also by others in patients with thalamic lesions 118, 25, 461. The higher frequency of reports of thalami~ astasia following thalamotomy may reflect the fact that the akinesia of Parkinson’s disease can be ag- gravated by thalamotomy 1471. Marsden 1481 has pos-

Masdeu and Gorelick: Thalamic Astasia 601

tulated that the basal ganglia are responsible for the automatic execution of learned motor plans. Our patients and others with thalamic lesions f9, 18, 191 pro- vide striking examples of impairment in the automatic execution of learned motm movements.

Sensory impairment may have contributed to the abnormalities of gait and station in our patients. Inabil- ity to stand despite minimal weakness has been described with severe bilateral peripheral sensory loss f49, SO]. 2011 attributed the impairment of balance after thalamotomy to proprioceptive loss 191. Some of our patients with protracted inability to stand had moderate to severe proprioceptive loss (Patients 2 and 6), but others did not (Patients 1, 3, and 7). Sensory loss correlated with involvement of the ventral posterior nucleus. If present, sensory loss aids in the localization of the lesion. In patients with astasia the presence of corticospinal tract or cerebellar-like findings and sensory loss on the same side renders a cerebellar localization unlikely and should suggest thalamic or suprathalamic involvement 121, 22, 25, 51, 52).

Other disorders of postural stability have been described with thalamic lesions. Hyperekplexia, the sudden loss of postural tone caused by startling stimuli, was exacerbated by a superimposed thalamic infarction {53]. Unilateral asterixis, which occurred in 4 of our patients, has been reported with lesions in the ventrolateral nucleus, but is not restricted to thalamic lesions [54-571. Both asterixis and thalamic astasia are manifestations of disordered postural tone. However, their relationship will remain unclear until more is known about the mechanisms underlying sustained muscle contraction in humans.

In summary, unilateral thalamic lesions, particularly those of an acute nature, can cause inability to walk or to sit up in alert patients with minimal or no weakness. The findings are transient, with resolution within days to weeks. The dorsothalamic region appears to be the underlying neuroanatomical locus that mediates the dysfunction. Because of the transient nature of thalamic astasia, it may have escaped emphasis in prior descriptions of the thalamic syndrome.

Dr Richard Kovner performed the neuropsychological evaluation of Patient 7. Dr Seymour Solomon referred Patient 14. Dr Steven Sparr obtained patient videorecordings. Dr Michael Grundman pro- vided valuable suggestions for the manuscript.

References 1. Dejerine J, Roussy G. Le syndrome thalamique. Rev Neurol

(Paris) 1906;14:521-532 2. Foix C, Hillemand P. Les syndromes de la region thalamique.

Presse Med 1925;33:113-117 3. Graff-Radford NR, Damasio H, Yamada T, et al. Nonhaemor-

rhagic thalamic infarction. Clinical, neuropsychological and elec- trophysiological findings in four anatomical groups defined by computerized tomography. Brain 1986; 108.485-5 16

4. Hirose G, Kosoegawa H, Saeki M, et al. The syndrome of posterior thalamic hemorrhage. Neurology 1985;35:998-1002

5. Kawahara N, Sato K, Muraki M, et al. CT classification of small thalamic hemorrhages and their clinical implications. Neurology

6. Martin JJ. Thalamic syndromes. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology. Amsterdam: North Holland,

7. Yakovlev PI. Localization of lesions of the thalamus. In: Hay- maker W, ed. Bing's local diagnosis in neurological diseases. St

8. Velasco F, Velasco M. A reticulothalamic system mediating proprioceptive attention and tremor in man. Neurosurgery

7. 2011 JG. Transient anosognosia associated with thalamotomy; is it caused by proprioceptive loss? Confin Neurol 1969;3 1:48-55

10. Hassler R. Thalamic regulation of muscle tone and the speed of movement. In: Purpura DP, Yahr MD, eds. The thalamus. New York: Columbia University Press, 1966:419-438

11. Schaltenbrand G, Wahren W. Atlas for stereotaxy of the human brain. Stuttgart, West Germany: Thieme, 1977

12. DeJong RN. Case taking and the neurologic examination. In: Baker AB, Joynt RJ, eds. Clinical neurology. Vol 1. Hagers- town, MD: Harper & Row, 1985:l-87

13. Goodglass H, Kaplan E. The assessment of aphasia and related disorders. Philadelphia: Lea & Febiger, 1972

14. Kaplan E, Goodglass H, Weintraub S. The Boston Naming Test. Boston: E. Kaplan and H. Goodglass, 1978

15. Mattis S . Dementia rating scale. In: Bellack R, Karasu B, eds. Geriatric psychiatry. New York, Grune, 1976:108-121

16. Friel JP. Dorland's illustrated medical dictionary. 25th ed. Phila- delphia: Saunders, 1974

17. DeJong RN. Case taking and the neurologic examination. In: Baker AB, Joynt RJ, eds. Clinical neurology. Vol 1. Hagers- town, MD: Har-Row, 1985:48

18. Cambier J, Elghozi D, Strube E. Gsions du thalamus droir avec syndrome de I'hkmisphere mineur. Discussion du concept de nkgligence thalamique. Rev Neurol (Paris) 1980;136:105-116

19. Laplane D, Escourolle R, Degos JD, et al. La nkgligence motrice d'origine thalamique. A propos de d e n cas. Rev Neurol (Paris)

20. Jenkyn LR, Alberti AR, Peters JD. Language dysfunction, somasthetic hemi-inattention, and thalamic hemorrhage in the dominant hemisphere. Neurology 1981;3 1:1202

2 1. Verma AK, Maheshwari MC. Hypesthetic-ataxic-hemiparesis in thalamic hemorrhage. Stroke 1986;17:49-51

22. Huang CY, Lui FS. Ataxic-hemiparesis, localization and clinical features. Stroke 1984 ; 1 5 : 3 6 3 -366

23. Iraqui VJ, McCutchen CB. Capsular ataxic hemiparesis. Arch Neurol 1982;39:528-529

24. Sage JI, Lepore FE. Ataxic hemiparesis from lesions of the corona radiata. Arch Neurol 1983;40:449-450

25. Fisher CM, Cole M. Homolateral ataxia and crural paresis; a vascular syndrome. J Neurol Neurosurg Psychiatry 1965;28:48-55

26. Groothuis DR, Duncan GW, Fisher CM. The human thala- mocortical sensory path in the internal capsule: evidence from a small capsular hemorrhage causing a pure sensory stroke. Ann Neurol 1977;2:328-333

27. Graff-Radford NR, Schelper RL, Ilinsky IA, Damasio H. Com- puted tomographic and postmortem study of a nonhemorrhagic thalamic infarction. Arch Neurol 1985;42:761-763

28. Masdeu JC, Fine M. Cerebrovascular disorders. In: Gonzalez CF, Grossman CB, Masdeu JC, eds. Head and spine imaging. New York: Wiley, 1985:283-356

1786;36:165-172

1969:469-496

Louis: Mosby, 1969:441-464

1979;4:30-36

1982;138:201-211

29. Jones EG. The thalamus. New York: Plenum Pr, 1985 30. Van Buren JM, Borke RC. Variations and connections of the

human thalamus. New York: Springer Verlag, 1972


3 1. Masdeu J, Wolfson L, Lantos G. CT scan findings in the elderly with frequent falls. Neurology 1986;36(suppl 1):104

32. Asanuma C, Thach WT, Jones EG. Distribution of cerebellar terminations and their relation to other afferent terminations in the thalamic ventral lateral region of the monkey. Brain Res Rev

33. Garcin R, Lapresle J. Incoordination ceribelleuse du membre infkrieur par lesion localisee dans la region interne du thalamus contro-lat&al. Rev Neurol (Paris) 1969;120:5-13

34. Chiray M, Foix C, Nicolesco J. Himitremblement du type de la scliose en plaques par 16sion rubro-thalamo-sous thalamique. Ann Med Interne (Paris) 1923;14:173-191

35. Sigwald J, Monnier M. Syndrome thalamo-hypothalamique avec hemitremblement (ramollissement du territoire artkriel thalamo-perfore). Rev Neurol (Paris) 1936;66:616-63 1

36. Brodal A. Neurological anatomy in relation to clinical medicine. 3rd ed. New York: Oxford University Press, 1981:257

37. Bogousslavsky J, Miklossy J, D e w JP, et al. Unilateral left paramedian infarction of thalamus and midbrain: a clinico- pathological study. J Neurol Neurosurg Psychiatry 1986;

38. Masdeu JC. The localization of lesions affecting the cerebral hemispheres. In: Brazis PW, Masdeu JC, Biller J, eds. Localiza- tion in clinical neurology. Boston: Little, Brown, 1985:301- 359

39. Watson RT, Heikqan KM. Thalamic neglect. Neurology 1979; 29:690-694

40. Watson RT, Valenstein E, Heilman KM. Thalamic neglect. Pos- sible role of the medial thalamus and nucleus reticularis in be- havior. Arch Neurol 1981;38:501-506

41. Graff-Radford NR, Eslinger PJ, Damasio AR, Yamada T. Nonhemorrhagic infarction of the thalamus: behavioral, ana- tomic, and physiologic correlates. Neurology 1984;34:14-23

42. Henderson VW, Alexander MP, Naeser MA. Right thalamic injury, impaired visuospatial perception, and alexia Neurology

43. Mohr JP, Watters WC, Duncan GW. Thalamic hemorrhage and

1983;5:237-265

49:686-694

1982;32:235-240

aphasia. Brain Lang 1975;2:3-17

44.

45.

46.

47.

48.

49.

50.

Cravioto H, Silverman J, Feigin I. A clinical and pathological study of akinetic mutism. Neurology 196O;lO:lO-21 Damasio AR, Damasio H, Chui HC. Neglect following damage to frontal lobe or basal ganglia. Neuropsychologia 1980;18:

Parisi JE, Collins GH, Kim RC, Crosley CJ. Prenatal symmetrical thalamic degeneration with flexion spasticity at birth. Ann Neurol 1983;13:94-97 Hassler R. Stereotactic brain surgery for extrapyramidal motor disturbances. In: Schaltenbrand G, Bailey P, eds. Introduction to stereotaxis with an atlas of the human brain. vol 1. Stuttgart, West Germany: Thieme, 1959 Marsden CD. The mysterious motor function of the basal ganglia: The Robert Warternberg Lecture. Neurology 1982;32: 5 14-539 Sobue G, Senda Y, Matsuoka Y, Sobue I. Sensory ataxia. A residual disability of Guillain-Barre syndrome. Arch Neurol

Albin RL, Albers JW, Greenberg HS, et al. Acute sensory neuropathy-neuronopathy from pyridoxine overdose. Neurol-

123-132

1983;40:86-89

ogy 1987 ; 3 7 : 1 7 29- 1 7 32 51. Jokelainen M, Pike A. Ataxic hemiparesis. Arch Neurol

52.

53.

54.

55.

56.

57.

1983;40:326 Perman GP, Racy A. Homolateral ataxia and crural paresis: case report. Neurology 30;1980:1013-1015 Fariello RG, Schwaraman RJ, Beall SS. Hyperekplexia exacerbated by occlusion of posterior thalamic arteries. Arch Neurol

Calzetti S , Gemignani F, Salati MR, Terzano MG. Unilateral asterixis due to thalamic nunor. Case report. Ital J Neurol Sci

Donat JR. Unilateral asterixis due to thalamic hemorrhage. Neurology 1980;30:83-84 Massey EW, Goodman JC, Stewart C , Brannon WL. Unilateral asterixis: motor integrative dysfunction in focal vascular disease. Neurology 1979;29:1188-1190 Young RR, Shahani BT. Asterixis: one type of negative myo- clonus. Adv Neurol 1986;43:137-156

1983 ;40:244-246

1983;1:87-90

Masdeu and Gorelick: Thalamic Astasia 603

thalamic astasia: inability to stand after unilateral thalamic lesions

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