(Stroke. 1996;27:1530-1536.)
© 1996 American Heart Association, Inc.
Articles |
Thalamic Vascular Lesions
Risk Factors and Clinical Course for Infarcts and Hemorrhages
the Laboratory of Cerebrovascular Pathology, National Institute of Neurology and Neurosurgery "Manuel Velasco Suarez," Mexico City, Mexico.
Correspondence to Juan Nader, MD, Laboratory of Cerebrovascular Pathology, National Institute of Neurology and Neurosurgery "Manuel Velasco Suarez," Insurgentes Sur No. 3877, CP 14269, Mexico City, Mexico.
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Abstract |
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Background and Purpose The data of patients with an MRI-confirmed diagnosis of thalamic stroke were analyzed to identify risk factors and to describe the clinical syndromes according to the thalamic arterial territory involved.
Methods We examined the records of all patients with a diagnosis of thalamic stroke confirmed by MRI who attended the National Institute of Neurology and Neurosurgery "Manuel Velasco Suarez" from 1987 through 1995. A database containing demographic features, risk factors, clinical course, type and mechanism of stroke, and vascular territory was analyzed.
Results Twenty-eight patients (19 men and 9 women; mean age, 48.2 years) had MRI-confirmed thalamic stroke. Infarct was present in 22 patients and hemorrhage in 6. Eleven (39.3%) patients were younger than 45 years. In these young patients, cigarette smoking was the main risk factor associated with the development of stroke. In young patients, isolated and multiple thalamic lesions were present in almost equal proportions. The remaining 17 patients were older adults (45 to 84 years of age). In such patients, most lesions were multiple and were associated with atherosclerosis-predisposing factors. The main distinguishing clinical feature for hemorrhages and paramedian infarcts in comparison with infarcts in the other thalamic territories was the presence of an altered level of consciousness. No patient died as a direct result of the stroke.
Conclusions Thalamic stroke commonly occurs in young adults, and its mechanism is often undetermined. Increased awareness of this type of stroke in young adults should lead to better delineation of its clinical features, course, and management.
Key Words: cerebral ischemia • hemorrhagic stroke • magnetic resonance imaging • thalamus • young adults
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Introduction |
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The thalamus is a diencephalic structure whose nuclei represent a gateway for input and output to and from the cerebral cortex. It receives, modifies, and relays information from major afferent, somatomotor, reticular formation, and limbic system pathways. The thalamus is supplied by four arterial systems, three derived from the vertebrobasilar system (paramedian thalamo-subthalamic, thalamogeniculate, and posterior choroidal arteries) and one derived from the posterior communicating artery (polar artery). Vascular lesions in each of these territories give rise to distinct clinical syndromes.1 2 3 4 5 6 7 8 9 10
With the advent of CT and more recently MRI, it has been shown that thalamic stroke is more common than previously believed.11 In addition, some differences in the epidemiology of stroke subtypes have been reported for populations of white, Asian, and Mesoamerican persons.12 13 14 15 16 We report the data from a series of patients with MRI-confirmed thalamic stroke, either infarct or hemorrhage, to identify risk factors and to describe clinical syndromes according to the arterial territory involved. We also discuss the mechanisms and course of the lesions and compare our findings with those reported in the literature.
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Subjects and Methods |
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We examined the records of all patients evaluated at the National Institute of Neurology and Neurosurgery with a diagnosis of thalamic stroke, either infarct or hemorrhage, confirmed by MRI from January 1987 through March 1995. All those patients belonged to the mestizo population of our country, which is a racial admixture of Spaniards and native Mexican Indians. Some of the patients had thalamic stroke before 1987 (as far back as 1976), but it was not until 1987 that the diagnosis was confirmed by MRI. A database was developed to record the following information: demographic features, risk factors, cardiac examinations, clinical course, type of stroke, mechanism, and vascular territory. Hypercholesterolemia was defined as cholesterol serum levels >5.2 mmol/L (220 mg/dL) and hypertension as blood pressure >160/90 mm Hg recorded at least twice before stroke. Cigarette smoking, diabetes mellitus, hypercholesterolemia, and hypertension were considered as atherosclerosis-predisposing factors for data analysis. The vascular territory involved was assessed using the templates proposed by Graff-Radford et al1 and Bogousslavsky.17 Statistical data on risk factors and stroke mechanism were analyzed by using
2 and Fisher's exact tests. Because of the small number of cases involved, the data on clinical course according to the vascular territory affected were analyzed using descriptive statistics. |
Results |
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There were 28 patients with thalamic stroke (Table 1
), 19 men and 9 women, with a median age of 48.2 years (range, 16 to 84 years). Thalamic infarct was present in 22 patients (78.6%) and thalamic hemorrhage in 6 (21.4%). The patients were divided according to age into two groups: young (15 to 44 years) or older (45 to 84 years) adults.18 Eleven (39.3%) of the 28 patients were young, and 17 (60.7%) were older adults. The median age for the young patients was 24.9 years, and all patients except 1 were men, with a ratio of men to women of 10:1 (P<.05). In this age group, 8 of the 11 strokes (72.7%) were ischemic and 3 (27.3%) were hemorrhagic. The median age for older adult patients was 59.7 years, with a ratio of men to women of 1:1. In this group, 14 of the 17 strokes (82.35%) were ischemic and 3 (17.65%) were hemorrhagic.
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Risk Factors
In young patients, smoking was the main risk factor associated with thalamic infarction (P=.05). Four of the 8 young patients with ischemic strokes were active smokers at the time of stroke. In 2 of the 4 active smokers, an additional atherosclerosis-predisposing factor was also present (hypercholesterolemia in 1, hypercholesterolemia and hypertension in the other). Additionally, 1 of the active smokers had a congenital ventricular septal defect. Of the remaining 4 patients, migraine was present in 2 (25%), 1 (12.5%) had rheumatic valvular disease (mitral stenosis), and the other had no known risk factors. The 3 young patients with thalamic hemorrhage had one or more atherosclerosis-predisposing factors. Two of these patients were hypertensive (1 had renovascular hypertension and the other had hypertension secondary to the use of sympathomimetic drugs).
In the 14 older adults with thalamic infarction, the risk factors were atherosclerosis-predisposing factors in 11 (78.5%) patients, 8 of whom were hypertensive (P<.05) (4 had hypertension alone; in the other 4 it was associated with diabetes mellitus and hypertensive cardiomyopathy; cigarette smoking, diabetes mellitus and hypercholesterolemia; and cigarette smoking, diabetes mellitus, and ischemic cardiomyopathy, respectively); 6 of the 14 patients (42.8%) had one or more cardiac disorders (ischemic cardiomyopathy in 3 and hypertensive cardiomyopathy, mitral stenosis with atrial fibrillation, and nonvalvular atrial fibrillation 1 each). Additionally, 2 of the 14 patients (14.2%) had had a previous transient ischemic attack. All 3 older adult patients with thalamic hemorrhage were hypertensive.
Isolated or Multiple Lesions
If the lesion affected only the thalamus, it was labeled as isolated. If it affected other territories in addition to the thalamus, it was labeled as multiple. Thalamic stroke was isolated in 11 of the 28 patients (39.3%) and multiple in 17 (60.7%). Three of the 6 patients with isolated thalamic infarct did not have any documented risk factor, whereas mitral stenosis, migraine, and atrial fibrillation were found in 1 patient each. In the group with isolated thalamic hemorrhage (n=5), all patients had atherosclerosis-predisposing factors, with hypertension being the only risk factor in 2 patients. Additionally, 1 of these 5 patients had suffered a previous transient ischemic attack manifested as right hemiparesis, and another patient had had an episode of transient global amnesia.
Of the 16 patients with multiple lesions and thalamic infarcts, 15 (93.7%) had atherosclerosis-predisposing factors such as cigarette smoking, diabetes mellitus, hypertension, or hypercholesterolemia, either isolated or in combination; 6 (37.5%) had cardiac disorders (ischemic cardiomyopathy in 3 and congenital ventricular septal communication, mitral stenosis with atrial fibrillation, and hypertensive cardiomyopathy in 1 patient each); 1 patient had migraine and 2 had a previous transient ischemic attack manifested as hemihypesthesia. The only hemorrhagic event in the multiple vascular disease group occurred in a patient with coagulopathy secondary to chronic liver failure.
In the 11 patients with isolated thalamic infarction, either younger or older adults, there were no predominant risk factors, whereas multiple thalamic infarcts were present to a greater degree in older adults (12 older versus 5 younger patients). The most important risk factors for the development of multiple thalamic strokes were again atherosclerosis-predisposing factors, either isolated or in combination (11 of 12 patients).
Stroke Mechanism
The cause of stroke was unknown in 3 of the 11 young patients. Cardioembolism, demonstrated by the presence of intracavitary thrombi during echocardiography, was the mechanism in 2 patients, in 1 in association with a ventricular septal defect and in the other with mitral stenosis. Small-vessel disease, as suggested by MRI, in the presence of hypertension was found in 1. Basilar artery dissection and vasculitis of unknown type, both suggested by angiography, were present in 1 patient each. Additionally, coagulopathy secondary to chronic liver disease, use of sympathomimetics, and renovascular hypertension were present in 1 patient each. The use of sympathomimetics was the presumed cause of stroke in 1 patient, since hypertension disappeared when the drug was discontinued, and there were no other risk factors for stroke (Table 2).
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In older adults, the main cause of stroke was large-vessel atherosclerosis, present in 5 of 15 patients. Cerebral atherosclerosis was suggested by angiography, in addition to the presence of atherosclerosis-predisposing factors. Small-vessel disease, demonstrated by MRI, in the presence of hypertension was found in 3; hypertensive hemorrhage was present in 3; cardioembolism, supported by the finding of intracavitary thrombi during echocardiography, was present in 2 patients, 1 with mitral stenosis, the other with atrial fibrillation; postangiography vasospasm was the cause of stroke in 1 patient (Table 2
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Vascular Territory
The most commonly affected vascular territory in all patients (both infarcts and hemorrhages) was the thalamogeniculate pedicle in 11 of the 28 patients (39.3%), followed in decreasing order by the paramedian thalamo-subthalamic artery territory in 7 (25%), the polar artery territory in 4 (14.3%), the entire thalamus in 4 (14.3%), and the posterior choroidal artery territory in 2 patients (7.1%). Fig 1 summarizes on redrawn templates the site and size of the thalamic lesions. Figs 2 through 4 are MRIs showing the extent of the lesion in three different territories: thalamogeniculate, paramedian thalamo-subthalamic, and the entire thalamus.
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Clinical Course for Infarcts
Thalamogeniculate Pedicle (n=11)
Five (45.4%) of the patients developed a complete thalamic syndrome with sensory and motor deficits and abnormal movements.4 In these 5 patients, the sensory deficit was the initial manifestation, followed by motor deficits. The abnormal movements appeared later, dominating the clinical course. Three patients (27.3%) developed sensorimotor stroke (paresthesia, or numbness on one side of the body with hemiparesis, increased reflexes, and an extensor plantar reflex); 2 patients (18.2%) developed pure motor abnormalities along with third cranial nerve involvement (with ptosis, diplopia, and ophthalmoparesis), and 1 patient (9.1%) developed a pure sensory deficit limited to the arm.19 20 Regarding speech and cognition, 2 patients (18.2%) had speech disturbances and 3 (27.3%) had memory impairment (anterograde amnesia in all cases). Three patients (27.3%) presented with stupor.
Paramedian Thalamo-Subthalamic Artery Territory (n=5)
Three patients (60%) had sensorimotor abnormalities, 2 of whom also had third cranial nerve involvement (diplopia, ophthalmoparesis, ptosis, and midriasis); one (20%) had pure motor abnormalities along with third cranial nerve involvement and abnormalities of vertical gaze. All 5 patients had an altered level of consciousness. In 1 patient, the altered level of consciousness was the only manifestation of stroke, with the patient presenting with alternating periods of stupor and alertness. One patient had speech disturbances and the other developed anterograde amnesia.
Polar Artery Territory (n=4)
Two patients (50%) had a pure motor deficit (in 1 patient it was associated with motor aphasia and in the other with anterograde amnesia), 1 patient presented with sensorimotor deficit with anterograde amnesia, and the other developed isolated third cranial nerve involvement with ptosis and diplopia.
Posterior Choroidal Artery Territory (n=2)
One patient had a pure motor deficit, whereas the other presented with sensorimotor deficit. Both patients had speech disturbances (motor aphasia in 1, dysarthria in the other).
Clinical Course for Hemorrhages
Global Thalamic Damage (n=4)
Three of the patients presented with an altered level of consciousness (coma in 2 patients and stupor in the other). Two of these patients had a sensorimotor deficit, and the other 2 had pure motor abnormalities. Additionally, memory impairment was present in 1.
Paramedian Thalamo-Subthalamic Territory (n=2)
Both patients had anterograde amnesia; 1 developed a sensorimotor deficit along with third cranial nerve involvement with ptosis, ophthalmoparesis, midriasis, and diplopia, whereas the other had a pure sensory deficit and anterograde amnesia.
Follow-up
The longest period of follow-up was 17 years and the shortest 3 months. None of the patients died as a result of stroke, but 1 patient with thalamic hemorrhage remained comatose until discharge. Most of the patients had persistent motor and sensory deficits, although 3 patients had no sequelae. Any neuropsychological alterations that remained after discharge were not described in hospital records, but 1 patient continued with "thalamic dementia" for several years until she was lost to follow-up.
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Discussion |
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Thalamic stroke became historically important after the initial description by Dejerine and Roussy.21 The incidence of thalamic hemorrhage varies from 8% to 35.4%, depending on the series studied.12 22 We found that thalamic strokes constitute 2.8% of all hemorrhagic strokes and 3.1% of all ischemic strokes at our institution.
Stroke in young patients accounts for 3% to 17% of all strokes.19 23 24 25 26 The young patients in our series represented 39.3% of all cases. The median age of our patients was 48.2 years, and thus they were younger than subjects of other studies in which median ages have varied from 61.7 to 68.5 years.10 27 28 We found a predominance of males in our young adults, unlike the Lausanne Stroke Registry15 in which females predominated in the extreme age groups (<30 and >80 years). The higher frequency of young patients with stroke in our population could be due in part to the fact that the median age of patients seen at our institution is lower than in other reported series.
For young patients, the most frequent causes of stroke are cardiogenic brain embolism (32%)25 and small-vessel disease (22%).19 These were the most frequent causes found in our series, both leading to stroke in 27.3% of our patients. Cigarette smoking was the most important risk factor for the development of ischemic stroke in 50% of young patients (P=.05), followed by migraine and heart disease in the other 50%. Cigarette smoking is an important risk factor for the development of atherosclerosis and stroke,26 29 30 especially when it is associated with hypertension and other atherosclerosis-predisposing factors.26 27 28 29 Migraine is a risk factor and also a potential cause of stroke when the stroke has a temporal relation with the migrainous event. In the present study, we lack the information regarding the time relationship between the migraine episode and stroke; thus, we could not consider migraine as the direct cause of stroke. Several studies31 32 33 34 have shown a high percentage of drug and alcohol abuse among young patients with stroke. These data are unknown for the population in our study, but in the absence of other risk factors that explain stroke in these young persons, it may be pertinent to conduct further toxicological studies in our young patients with stroke.
In accordance with other studies,26 35 the main risk factor for ischemic and hemorrhagic stroke in older adults was hypertension (P<.05), either isolated or accompanying other atherosclerosis-predisposing factors. Thus, treatment of high blood pressure, even in mild hypertension, needs to be encouraged.
Most of the cases of thalamic stroke were associated with infarcts in other territories (60.7%), whereas isolated lesions were only present in 39.3% of cases. Multiple lesions, related to the presence of a greater number of risk factors (especially atherosclerosis-predisposing factors), were more common in older than in younger adult patients (P<.05). It would be expected that isolated lesions would be more common in the younger group of patients, but the results demonstrate that isolated thalamic lesions occurred in the same proportion in younger and older adult patients. Other risk factors need to be sought to explain the similar rates of isolated thalamic stroke in both age groups.
In the present study, the vascular territories affected by thalamic stroke had the same distribution as that described by Bogousslavsky et al.11 17 The finding that the thalamogeniculate pedicle is the most commonly affected territory is attributed to the arterial or arteriolar changes related to hypertensive arteriolopathy that are frequently observed in this region.27
The patients with lesions in both the thalamogeniculate and the paramedian thalamo-subthalamic artery territories followed the classic clinical course described for these lesions.1 4 5 6 8 An important number of our patients with lesions in the thalamogeniculate territory had the clinical course of the complete thalamic syndrome, including sensory and motor deficits with the presence of abnormal movements. A change in the level of consciousness is rare with lesions in this territory, but we found changes in our patients with multiple lesions (some of the additional lesions were located in the brain stem). All of our patients with lesions in the paramedian thalamo-subthalamic artery territory had altered levels of consciousness, a predominant finding and an important component of the classic triad for these lesions (acute decrease in level of consciousness, cognitive and behavioral abnormalities, and abnormalities of vertical gaze).4 8 Additionally, the majority had third cranial nerve involvement with vertical gaze impairment. One of our patients with bilateral infarct in this territory had thalamic dementia, a finding that is in accordance with reports describing dementia as a manifestation of bilateral paramedian thalamo-subthalamic infarct.6 36
The patients with lesions in the polar and posterior choroidal territories did not follow the classic clinical course, in which neuropsychological disturbances would be the most common finding.2 37 It is important to state that all the lesions in the polar territory of our patients were multiple, and this could explain why these patients presented with motor deficits. The lack of neuropsychological findings in our patients could be explained by the absence of standardized psychological evaluation in this retrospective study. The development of third cranial nerve involvement in 1 of our patients with a vascular lesion in the polar artery territory may be explained by the fact that in some individuals the polar artery is absent and its territory is supplied by the paramedian thalamo-subthalamic artery.1 4 As for the posterior choroidal territory lesions, the most common clinical signs are sectoranopias or quadrantanopias. These patients occasionally present with slight hemiparesis or hemihypesthesia. In our series, 1 patient had left hemiparesis-hemihypesthesia, whereas the other was quadriparetic.
In regard to the hemorrhagic events, patients with lesions that were small and circumscribed to the paramedian thalamo-subthalamic artery territory showed no difference to those patients with ischemic lesions in this territory. When our patients had larger hemorrhagic events, they did not present with a specific clinical profile but with a combination of motor and sensory abnormalities and an altered level of consciousness. An altered level of consciousness was common both for hemorrhagic and ischemic strokes in the paramedian thalamo-subthalamic territory. This feature may serve to distinguish hemorrhagic and ischemic paramedian strokes from ischemic strokes in the other thalamic territories, where an altered level of consciousness is not common (P<.005).
The prognosis of thalamic stroke is worse if the event is hemorrhagic, in that the level of consciousness is often decreased.9 10 We found that 1 patient with thalamic hemorrhage remained comatose, whereas all other patients, including those with paramedian thalamic infarction, recovered to a normal state of consciousness. Neuropsychological abnormalities are permanent in a great percentage of patients.37 However, neuropsychological abnormalities in our series were confined to 1 patient with bilateral paramedian infarcts who developed thalamic dementia.
This retrospective study of MRI-proven diagnosis of thalamic stroke has provided us with information on the epidemiology, mechanism, and clinical features of thalamic stroke in our population. The absence of a clear causative mechanism in young patients in our series indicates that this population may be exposed to risk factors that have not yet been fully elucidated.
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Acknowledgments |
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This work was partially sponsored by the "Consejo Nacional de Ciencia y Tecnologia" of Mexico (CONACYT). We thank Linda Stopp for her help in translation and style corrections and Samuel Maganon for his help with the analysis of data.
Received January 9, 1996; revision received June 5, 1996; accepted June 5, 1996.
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References |
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