(Stroke. 1995;26:964-970.)
© 1995 American Heart Association, Inc.
Articles |
Thalamic Hemorrhage
A Prospective Study of 100 Patients
From the Departments of Neurology (E.K., T.K., K.K.) and Social and Statistical Sciences (N.O.E.), Ege University Faculty of Medicine, Bornova, Izmir, Turkey.
Correspondence to Emre Kumral, MD, Neurology Department, Ege University Faculty of Medicine, Bornova, Izmir, Turkey.
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Abstract |
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Background and Purpose The clinical features of thalamic hemorrhage in terms of localization are of great interest in many studies. To better understand the relationship between the localization of thalamic hemorrhage and clinical features, we evaluated the characteristics of patients with four different topographic types of thalamic hemorrhage.
Methods We prospectively studied 100 patients with thalamic hemorrhage who were admitted consecutively to our primary care unit. We divided them into two groups according to large (>2 cm in diameter and/or >4 mL in volume) and small thalamic hemorrhage. Four topographic subgroups (large and small) were compared to identify clinical syndromes associated with distinct lesion locations.
Results All patients with posterolateral thalamic hemorrhage had severe sensorimotor deficit. Neuropsychological disturbances in patients with posterolateral thalamic hemorrhage were prominent, with primarily transcortical aphasia in those with left-sided lesions and hemineglect and anosognosia in those with right-sided lesions. Several variants of vertical gaze dysfunction, skew ocular deviation, gaze preference toward the site of the lesion, and miotic pupils were frequent in posterolateral thalamic hemorrhage, particularly in the large type. Patients with small and large anterolateral thalamic hemorrhage were characterized by severe motor and sensory deficits; language and oculomotor disturbances were also observed, although less frequently than in posterolateral hemorrhage. Sensorimotor deficits were observed in patients with medial thalamic hemorrhage (moderate in small hemorrhages and severe in large hemorrhages because of involvement of the adjacent internal capsule). Language disturbances in patients with left-sided lesions and neglect in patients with right-sided lesions were seen only in large medial thalamic hemorrhage. Dorsal thalamic hemorrhage was rare and characterized by mild and transient sensorimotor disturbances. Among patients with dorsal thalamic hemorrhages, only those with large lesions had oculomotor and neuropsychological disturbances.
Conclusions We concluded that despite clinical similarity among the four types of thalamic hemorrhage, there was some discrepancy in the clinical features of small and large thalamic hemorrhages. The most important predictors of death were initial consciousness, nuchal rigidity, maximum size, volume and ventricular extension of hemorrhage, and occurrence of hydrocephalus.
Key Words: aphasia • prognosis • thalamus
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Introduction |
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At the beginning of this century Dejerine and Roussy1 provided a detailed description of thalamic syndrome. Thereafter, in 1925 Lhermitte2 and in 1930 Baudouin et al3 made important contributions toward defining the characteristics of thalamic hemorrhage. Fisher4 emphasized language disorders and ocular motility disturbances in thalamic hemorrhage. Recent advances in the field of radiology yielded accurate diagnoses and enabled the analysis of clinical characteristics and pathology without autopsy study. The clinical and radiological features and prognosis of thalamic hemorrhage have been reported in more recent studies. Different case reports have focused on distinct deficits in thalamic hemorrhages.5 6 7 8 9 10 11 12 13 14 15 16 In this study we attempted to evaluate the characteristics of 100 patients with four different topographic types of thalamic hemorrhage in regard to sensorimotor, oculomotor, and neurobehavioral deficits and factors affecting outcome.
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Subjects and Methods |
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We studied all patients admitted to our population-based center with the diagnosis of thalamic hemorrhage between January 1988 and December 1993. These patients represented a subsample of 4500 patients (4110 patients with ischemic stroke and 390 patients with hemorrhagic stroke) admitted to the Neurology Department of Ege University, which is a primary care unit for stroke patients in our region. Our patients with thalamic hemorrhage represented one fourth of all hemorrhagic cases. We investigated all patients with a standard protocol of investigations including blood and urine tests and brain CT (at least one scan between 1 and 5 days after stroke). We determined the precise location of each hemorrhage by the atlas of Schaltenbrand and Wahren17 using the sagittal reconstruction technique with 10-mm-thick transverse sections. We assessed maximum size (diameter) and volume and extension (superior, inferior, or lateral) of the thalamic hemorrhage in all patients. For clinicotopographic analysis, we determined four types of thalamic hemorrhage, as described elsewhere: anterolateral (including ventroanterior and ventrolateral nuclei), posterolateral (including posteroventrolateral and pulvinar nuclei), medial (including dorsomedial and intralaminar nuclei), and dorsal (including mainly dorsomedial nucleus) (Figure
).18 19
Hemorrhages larger than 2 cm in diameter and/or 4 mL in volume were
classified as large. All patients were examined by at least two senior
stroke neurologists (E.K., K.K.). The consciousness of patients was
assessed by the Glasgow Coma Scale (GCS). Sensory examination included
light touch (long-fibered cotton), superficial pain (pinprick),
position sense (passive movements of fingers and toes), vibration
(128-Hz tuning fork), streognosis (identification of a coin, pencil, or
key), and graphesthesia (recognition of letters or numbers written on
the tips of fingers and toes). Motor weakness in the face and upper and
lower limbs as well as other neurological disturbances were also
recorded. The language test was conducted by the Gülhane Aphasia
Test (GAT; in Turkish),20 which included fluency, oral and
writing comprehension, repetition, writing, and reading. A right
hemisphere test was performed by determination of gnosia of hemibody,
line bisection tests, and simultaneous application of auditive,
tactile, and visual stimuli.
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We investigated risk factors and concomitant diseases such as hypertension (blood pressure >160/90 mm Hg at least twice before stroke), arteriovenous malformation (in suspected cases assessed by conventional angiography or MRI), diabetes mellitus (fasting blood glucose level >6.0 mmol/L known to exist before stroke), cardiac disease, and previous transient ischemic attack (TIA). We evaluated the outcome of all patients 1 month after the stroke. Hemorrhage-related neurological syndromes were assessed on average 1 month after stroke.
Nonparametric median tests for median values of continuous variables,
2 test of association, and multiple regression
analysis were used to determine the factors affecting
intraventricular hemorrhage and death. Four topographic subgroups were
compared descriptively to identify clinical syndromes associated with
distinct lesion locations. MANOVA was performed to determine the
factors affecting consciousness and outcome in the first month after
stroke.
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Results |
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Our study group included 100 patients (66 females, 34 males; median age, 64±12.1 years; range, 16 to 90 years). Forty-nine percent of patients had left thalamic hemorrhage (12 anterolateral, 27 posterolateral, 7 medial, and 3 dorsal), and 51% of patients had right thalamic hemorrhage (9 anterolateral, 28 posterolateral, 8 medial, and 6 dorsal). We observed 21 patients with anterolateral, 55 with posterolateral, 15 with medial, and 9 with dorsal thalamic hemorrhage. Thirty-three patients had small thalamic hemorrhage (7 anterolateral, 16 posterolateral, 8 medial, and 2 dorsal), and 67 patients had large hemorrhage (14 anterolateral, 39 posterolateral, 7 medial, and 7 dorsal). In all patients the onset of stroke had occurred during daily activities. Seven patients had frontal headache at the onset of stroke. Seventy-four percent of patients had hypertension, 10% had diabetes, and 4% had previous ischemic stroke. We performed MRI on 16 patients and conventional angiography on 10 patients in whom we could not find any risk factor for thalamic hemorrhage. We did not find any pathology in these cases. Fifty-seven percent of patients had intraventricular hemorrhage, and 45% had nuchal rigidity, vomiting, and headache. Sixty-seven percent (45/67) of patients with large thalamic hemorrhage had intraventricular hemorrhage (25 patients with posterolateral, 8 with anterolateral, 7 with medial hemorrhage, and 5 with dorsal thalamic hemorrhage), and 36% (12/33) with small thalamic hemorrhage (2 patients with anterolateral, 6 with posterolateral, 3 with medial, and 1 with dorsal thalamic hemorrhage) had intraventricular hemorrhage. Intraventricular hemorrhage was correlated significantly with maximum size, volume, and extension to other areas (r=-.29, r=-.43, and r=.39, respectively). Twenty-one patients (37%) with intraventricular hemorrhage died. Thirty-eight patients (67%) with intraventricular hemorrhage developed acute hydrocephalus in 1 week, and 15 (39%) of them died within 1 month (P<.03). None of the patients had seizure at onset of stroke.
Stupor and coma were observed in 16 patients (29%) with
posterolateral, in 3 patients (14%) with anterolateral, in 2 patients
(13%) with medial, and in 2 patients (22%) with dorsal thalamic
hemorrhage. The smallest lesion that produced stupor or coma was 2 cm
in diameter (1.7 mL in volume) in 1 patient with posterolateral
thalamic hemorrhage. We observed stupor or coma (GCS score, 
8) in 3
patients (9%) with small thalamic hemorrhage (of the posterolateral
type) and in 20 patients (30%) with large thalamic hemorrhage (13
posterolateral, 3 anterolateral, 2 medial, and 2 dorsal). Five patients
(15%) with small thalamic hemorrhage and 16 patients (24%) with large
thalamic hemorrhage had a GCS score of 10 to 14. Seventy-six percent
(25/33) of the patients with small thalamic hemorrhage and 46% (31/67)
of the patients with large hemorrhage had normal consciousness (GCS
score, 15) (P<.001). MANOVA demonstrated a significant
correlation between consciousness and size, volume, and extension
(F=4.44, P=.007). Thirty-nine percent (9/23) of patients
with a GCS score 8 died, while only 21% (16/77) of patients with a
score 
9 died (P<.001) (Table 1).
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Neurobehavioral Findings
At the onset of stroke, 3 patients with large and 1 with small
hemorrhage had mutism, 7 patients with large thalamic hemorrhage
demonstrated global aphasia, and 6 patients had nonfluent speech
(Broca's aphasia) with impairment of repetition (3 with posterolateral
and 3 with medial thalamic hemorrhage). Transcortical aphasia, which
was characterized by hypophonia, reduced ouput, verbal paraphasia,
moderate impairment of comprehension, and preserved repetition, was
found in 20 patients with left thalamic hemorrhage (17 with large
thalamic hemorrhage). Six patients had dysarthria (4 with large
hemorrhage). Twenty percent (10/51) of patients with right thalamic
hemorrhage had anosognosia for hemiplegia (9 with large thalamic
hemorrhage), and 33% (17/51) had anosognosia and impairment of
visuospatial neglect contralateral to the thalamic hemorrhage (66%
with large thalamic hemorrhage). We found visuospatial neglect alone in
2 patients. Tactile and visual extinction were present in 27%
(14/51) of the patients with right thalamic hemorrhage (8
posterolateral, 4 anterolateral, and 2 dorsal), and auditive extinction
was observed in 10 patients with right large thalamic hemorrhage (7
posterolateral, 2 anterolateral, and 1 medial). During the acute state,
3 patients exhibited acute hallucinosis and agitation. One month after
stroke, 1 patient with large posterolateral thalamic hemorrhage
demonstrated a demential syndrome, and akinetic mutism occurred in 2
patients with large posterolateral thalamic hemorrhage 6 months later
(Table 2).
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Sensorimotor Findings
All patients had motor deficit at onset. Nineteen percent of
patients had moderate hemiparesis (4 with small posterolateral, 1 with
either small or large anterolateral, 8 with small medial, and 2 with
small and 3 with large dorsal hemorrhage), 11% had very mild motor
impairment (4 with small posterolateral, 1 with small and 2 with large
anterolateral hemorrhage, and 4 with large dorsal hemorrhage), and 70%
had hemiplegia (8 with small and 39 with large posterolateral, 5 with
small and 11 with large anterolateral, and 7 with large medial thalamic
hemorrhage). Ataxia was observed in 20 patients (10 with
posterolateral, 3 with anterolateral, 5 with medial, and 2 with dorsal
thalamic hemorrhage); 16 patients (80%) had large and 4 patients had
small thalamic hemorrhage. Sensory deficits could be detected in 66
patients; 13 had only superficial sensory deficit, and 53 patients had
a combination of superficial, deep, and cortical sensory deficits.
Among 13 patients with superficial sensory deficit, 12 patients had
posterolateral hemorrhage (10 with large and 2 with small thalamic
hemorrhage), and 1 patient had large anterolateral hemorrhage. Two
patients showed facial sensory deficit (1 with large posterolateral and
1 with small medial hemorrhage), 5 patients with large thalamic
hemorrhage had upper and lower extremities sensory deficits (1 with
anterolateral and 4 with posterolateral hemorrhage), 58 patients had a
complete sensory deficit involving the face and upper and lower limbs
(14 with anterolateral, 31 with posterolateral, 5 with medial, and 8
with dorsal thalamic hemorrhage), and 1 patient with large medial
thalamic hemorrhage had complete faciobrachial sensory deficit at the
beginning of stroke but 1 month later showed a sensory deficit only in
the cheiro-oral area.
Ocular Findings
In patients with posterolateral, anterolateral, and medial
thalamic hemorrhage, ocular signs were prominent and numerous. Gaze
preference toward the lesion was observed in 18 patients (72% with
large thalamic hemorrhage), 12 of whom (67%) had posterolateral
hemorrhage. Contralateral gaze preference was found to be present
in 5 patients with large thalamic hemorrhage (4 posterolateral and 1
anterolateral hemorrhage with inferior extension). Horizontal gaze
palsy was present in 9 patients (7 patients with large hemorrhage).
The most common oculomotor disturbance was upward gaze palsy (36%).
Forty-eight percent (32/67) of patients with large thalamic hemorrhage
had upward gaze palsy, whereas it was seen in only 12% (4/33) of
patients with small thalamic hemorrhage (P<.001). Eleven
patients had upward/downward gaze palsy. Only 1 patient with large
posterolateral hemorrhage had vertical 1.5 syndrome. Skew ocular
deviation was present in 31% (17/55) of patients with
posterolateral thalamic hemorrhage, 14 of whom had large thalamic
hemorrhage. One patient with large posterolateral thalamic hemorrhage
demonstrated tip-of-nose syndrome. Fixed pupils were seen in 21
patients with posterolateral hemorrhage; 16 patients had large
posterolateral hemorrhage, and 5 patients had small thalamic
hemorrhage. Three patients had hemianopia in the contralateral space
(Table 3).
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Thalamic Syndromes
The rare thalamic syndromes related to thalamic hemorrhage are
delineated in Table 4. No patient had acute thalamic
pain. One month after the stroke, 3 patients had only thalamic pain, 1
patient had choreiform movements, and some patients had combined
syndromes such as thalamic pain plus chorea plus ataxia (6 patients)
and thalamic hand plus asterixis (1 patient).
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Outcome
At 1 month after stroke, 25% of patients were dead. The death
rate was significantly correlated with initial consciousness
(r=-.57, P<.01), maximum size
(r=.56, P<.01), volume (r=.50,
P<.01), ventricular hemorrhage (r=.36,
P<.01), hydrocephalus (r=-.29,
P<.01), and nuchal rigidity (r=-.20,
P<.05). Topographic distributions of death due to thalamic
hemorrhage were as follows: 68% of patients with posterolateral
hemorrhage (15 with large and 2 with small hemorrhage), 16% of
patients with anterolateral hemorrhage (4 with large hemorrhage), and
8% of patients with either medial or dorsal hemorrhage (2 with large
hemorrhage). We observed death in 2 patients (6%) with small and 23
patients (34%) with large thalamic hemorrhage (Table 5). One month after stroke, outcome was dependent on
size (diameter) (P<.005), volume (P<.0003), and
extension (P<.02) of thalamic hemorrhage. One patient had
convulsions after the first month.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In the present study we attempted to determine different clinical aspects of thalamic hemorrhage in terms of topographic characteristics and effect of hemorrhage on outcome. Almost all patients had stroke during daily activities, and this reflects the previously reported circadian characteristic of hemorrhage frequency.21 Headache frequency in our study corresponds to the low frequency of initial headache in three other series.18 22 23 In fact, at admission all subjects had motor disability. In different studies, rates of motor disturbances were reported between 93% and 100%.18 23 24 In these patients both direct and indirect involvement of the adjacent internal capsule were frequent. Sensory deficit was almost complete in all patients. Similarly, other studies reported the most striking initial characteristics of thalamic hemorrhage to be hemiplegia/hemiparesis and contralateral sensory deficits, vomiting, headache, oculomotor disturbances, and neurobehavioral disturbances.4 18 We did not observe pure sensory stroke due to thalamic hemorrhage, although it has been reported.25 The clinical differentiation between thalamic and pseudothalamic parietal sensory stroke cannot be made on the basis of sensory deficits alone.26
Hypertension was the most frequent cause of thalamic hemorrhage in our patients (74%), and this result was similar to previous studies that indicated that hypertension was the major risk factor for intracerebral hemorrhage.27 Moreover, we observed that at admission blood pressure was higher in the majority of cases. This observation was also reported by several authors and may be explained by an autonomic response to increased intracranial pressure to maintain adequate cerebral perfusion.28 Frequency of diabetes was not higher in our series but was an important risk factor for ischemic thalamic stroke.29 30
Coma and stupor at onset have clearly been associated with fatal outcome in thalamic hemorrhages. Our findings demonstrated that stuporous or comatose patients were more frequently dead (39%) by the time of initial examination. Previous studies reported that initially comatose patients had the poorest chance of survival.22 23 24 We also observed that large thalamic hemorrhages can yield more disturbances in vigilance than small thalamic hemorrhages.
In our series one third of patients with intraventricular hemorrhage were dead within 1 month. The mortality rate in patients with intraventricular hemorrhage varied between 44% and 100%.22 23 24 31 Steinke et al18 reported that stroke-related deaths occurred in 52% of intraventricular hemorrhage cases, 13% of restricted intrathalamic hemorrhage cases, and in none of the cases of thalamic infarction.
In several studies maximum size of thalamic hemorrhage was another important factor determining outcome.3 18 22 23 Some authors reported that patients with thalamic hemorrhages exceeding 3.3 cm in diameter died within 1 month after stroke,22 23 24 but in our study 1 patient with 3.3-cm-diameter and 2 patients with 3.6-cm-diameter thalamic hemorrhage proved to be exceptions, and they survived and were able to lead an independent life 1 month after stroke. Multiple regression analysis demonstrated that size, intraventricular extension, and increased pulse pressure were independent predictors for mortality in supratentorial hemorrhage.32 33 34 Our MANOVA demonstrated that maximum size (diameter), volume, and extension of thalamic hemorrhage were independent predictors of outcome at 1 month after stroke.
In the present study we classified thalamic hemorrhage in four main topographic locations by categorizing them as large or small thalamic hemorrhage. All patients with posterolateral thalamic hemorrhage had sensorimotor deficit. Patients with small posterolateral thalamic hemorrhage demonstrated hemiparesis and hemiplegia equally, but patients with large thalamic hemorrhage had only severe motor deficit. Neuropsychological disturbances in patients with posterolateral thalamic hemorrhage were prominent, with primarily transcortical aphasia in those with left-sided lesions and hemineglect and anosognosia in those with right-sided lesions. The frequency of these disorders increased with the size of thalamic hemorrhage. The involvement of other nuclei such as anterior and dorsomedial nucleus and of capsulostriatal structures may explain the higher frequency of language disturbances and neglect.9 Several variants of vertical gaze dysfunction, skew ocular deviation, gaze preference toward the lesion, and miotic pupils are frequent in posterolateral thalamic hemorrhage, particularly in large hemorrhages. The outcome of patients with small posterolateral thalamic hemorrhage is better than that of patients with large thalamic hemorrhage.
Patients with small and large anterolateral thalamic hemorrhage were characterized by severe motor and sensory deficits. Language and oculomotor disturbances were observed but less frequently than in those with posterolateral hemorrhage. The outcome of patients with large anterolateral thalamic hemorrhage was worse than that of patients with small thalamic hemorrhage.
Sensorimotor deficits were also observed in patients with medial thalamic hemorrhage (moderate in small and severe in large hemorrhage because of involvement of the adjacent internal capsule). Language disturbances in patients with left-sided lesions and neglect in those with right-sided lesions were seen only in those with large medial thalamic hemorrhage, perhaps as a result of involvement of adjacent nuclei as lateral posterior, centromedial, and ventrolateral nuclei.
Dorsal thalamic hemorrhage is rare and is characterized by mild and transient sensorimotor disturbances. Among those with dorsal thalamic hemorrhages, only patients with large lesions had oculomotor and neuropsychological disturbances. These signs could be explained by the secondary pressure effect of hemorrhage.
We found that upward gaze palsy, fixed miotic pupils, gaze preference toward the lesion, and skew ocular deviation were frequent in patients with thalamic hemorrhage. In previous reports the most frequent oculomotor findings were impaired vertical gaze, small sluggish or reactive pupils, and horizontal gaze palsy.24 35 36 37 Vertical gaze palsy was reported in 34% to 94%, convergence spasm in 30%, and miosis in 70% of patients with thalamic hemorrhage.22 23 We observed gaze preference toward thalamic hemorrhage in 20% of our patients. The mechanism of the horizontal gaze disturbances is interruption of the descending fibers from the frontal eye field at the posterior thalamus, near the dorsal medial nuclei, internal medullary lamina, or medial pulvinar. Vertical gaze, convergence disorders, and several variants of vertical gaze dysfunction result from involvement of the intralaminar and part of the dorsomedial nucleus, along with coexisting lesions of the upper midbrain (rostral interstitial nucleus of the median longitudinal fasciculus and posterior commissure). Ipsilateral or bilateral miosis and ptosis in patients with thalamic hemorrhage could have been due to compression of the hypothalamus or descending sympathetic fibers.36 37 We observed one patient with the "tip-of-nose" syndrome, and in this case the hemorrhage extended into and compressed the midbrain. Forced downward deviation of the eyes might represent either an irritative effect of hemorrhage on structures responsible for downward gaze or imbalance created by an acute upgaze palsy.
Another aspect of thalamic hemorrhage is neurobehavioral disturbances consisting of language deficits, disorientation, memory disturbance associated with dominant lesions, and impaired visuoperceptual ability associated with nondominant lesions. Within these syndromes, many cases range in severity from "a few paraphasic errors to a complete receptive and expressive disorder."38 39 In an analysis of aphasic symptoms and topography of the affected thalamic nuclei, the pulvinar and the ventral-posterolateral nuclei were most frequently involved. The mechanism of different types of aphasia was explained as a disruption of any circuit (arranged as frontal rostrocaudal/thalamic mediolaterally) leading to dysfunction.9
In this study half of the patients with right thalamic hemorrhage had anosognosia and visuospatial neglect. In nondominant thalamic hemorrhage, impaired body schema, anosognosia for hemiplegia, hemineglect, and impaired visuospatial performance have primarily been reported.40 It was proposed that involvement of the medial thalamic nuclei induced hemispatial neglect due to disturbance of the arousal system.40 41 42 43 The currently most widely accepted hypothesis is that a thalamic lesion produces hemineglect by interrupting the ipsilateral corticolimbic-reticular activating loop at the subcortical level. It has been suggested that deficits in visuospatial attention are caused by involvement of the posterolateral, centromedial, and ventrolateral nuclei.42 43
In this series we found only six patients whose characteristics were similar to the classic syndrome of Dejerine and Roussy,1 which is rare. Thalamic pain in patients with large dorsal and medial hemorrhages may be explained by the effect of the size of hemorrhage. In the first week after acute stroke we did not observe any acute pain, but 1 month after stroke the classic thalamic syndrome appeared. This may be explained by inappropriate reorganization of the intrathalamic or extrathalamic neuronal network.
In conclusion, we suggest that differences exist despite the clinical similarity among the four types of thalamic hemorrhage. Large posterolateral thalamic hemorrhage leads to severe sensorimotor deficit and various oculomotor and neurobehavioral disturbances. Anterolateral thalamic hemorrhage has a clinical presentation that is similar to that of posterolateral thalamic hemorrhage, and large medial thalamic hemorrhage is particularly characterized by neuropsychological disturbances. Patients with dorsal thalamic hemorrhage exhibit mild and transient sensorimotor and neuropsychological deficits.
Received December 23, 1994; revision received February 16, 1995; accepted March 10, 1995.
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H.-O. Karnath, L. Johannsen, D. Broetz, and W. Kuker Posterior thalamic hemorrhage induces "pusher syndrome" Neurology, March 22, 2005; 64(6): 1014 - 1019. [Abstract] [Full Text] [PDF]
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K. Vestergaard, G. Andersen, H. Gottrup, B.T. Kristensen, and T.S. Jensen Lamotrigine for central poststroke pain: A randomized controlled trial Neurology, January 23, 2001; 56(2): 184 - 190. [Abstract] [Full Text] [PDF]
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T. G. Phan, M. Koh, R. A. Vierkant, and E. F.M. Wijdicks Hydrocephalus Is a Determinant of Early Mortality in Putaminal Hemorrhage Stroke, September 1, 2000; 31(9): 2157 - 2162. [Abstract] [Full Text] [PDF]
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I. Miyai, T. Suzuki, J. Kang, and B. T. Volpe Improved Functional Outcome in Patients With Hemorrhagic Stroke in Putamen and Thalamus Compared With Those With Stroke Restricted to the Putamen or Thalamus Stroke, June 1, 2000; 31(6): 1365 - 1369. [Abstract] [Full Text] [PDF]
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A. Bowen, K. McKenna, and R. C. Tallis Reasons for Variability in the Reported Rate of Occurrence of Unilateral Spatial Neglect After Stroke Stroke, June 1, 1999; 30(6): 1196 - 1202. [Abstract] [Full Text] [PDF]
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