Sensory Stroke Research Articles

Clinical lacunar syndromes as predictors of lacunar infarcts. A comparison of acute clinical lacunar syndromes and findings on diffusion-weighted MRI.

To evaluate if patients with acute lacunar syndromes have acute lacunar infarcts or other types of cerebral lesions on diffusion-weighted MRI. Patients with acute lacunar syndromes underwent echo-planar diffusion MRI of the brain within 3 days after stroke onset. Localization and size of lesions with hyperintense signal were determined, compared with clinical characteristics and with findings on follow-up T2-weighted MRI. Twenty-three patients participated in the study. Thirteen patients had pure motor stroke, 1 pure sensory stroke, 8 sensorimotor stroke, and 1 ataxic hemiparesis. Twenty-two patients had at least one lesion with increased signal on diffusion-weighted MR images. These acute lesions were in the internal capsule/ basal ganglia/thalamus in 13 patients, subcortical white matter in 5 patients, brainstem in 2 patients, cortex (multiple small lesions) in 1 patient, and cortex + basal ganglia in 1 patient. The median volume of the lesions was 0.6 ml on the initial examination and on follow-up, of 17 patients after 1 to 5 months, 0.5 ml. Almost all patients with acute ischemic lacunar syndromes have acute lesions on echo-planar diffusion-weighted MRI within 3 days after stroke onset. These lesions are mostly small and subcortical, compatible with lacunar infarcts caused by single penetrating artery occlusion, but in a minor proportion of patients (2 of 23 in our study) a cortical involvement is found.

Somatosensory evoked magnetic fields from the primary somatosensory cortex (SI) in acute stroke

We recorded somatosensory evoked magnetic fields (SEFs) to median nerve stimulation from 15 patients in the acute stage (1–15 days from the onset of the symptoms) of their first-ever unilateral stroke involving sensorimotor cortical and/or subcortical structures in the territory of the middle cerebral artery (MCA). Neuronal activity corresponding to the peaks of the N20m, P35m and P60m SEF deflections from the contralateral primary somatosensory cortex (SI) was modelled with equivalent current dipoles (ECDs), the locations and strengths of which were compared with those of an age-matched normal population. Four patients with pure motor stroke had symmetric SEFs. In one of the 4 patients with pure sensory stroke, and in 5 of the 7 patients with sensorimotor paresis, the SEFs were markedly attenuated or missing. All except one patient with abnormal SEFs had deficient two-point discrimination ability; especially the attenuation of N20m was more clearly correlated with two-point discrimination than with joint-position or vibration senses. Of the different SEF deflections, P35m and P60m were slightly more sensitive indicators of abnormality than N20m, the former being affected in two patients with symmetric N20m. Three patients with pure sensory stroke and lesions in the opercular cortex had normal SEFs from SI. We conclude that the SEF deflections N20m, P35m and P60m from SI are related to cutaneous sensation, in particular discriminative to touch. The results also demonstrate that basic somatosensory perception can be affected by lesions in the opercular cortex in patients with functionally intact SI.

Unilateral saccadic pursuit in patients with sensory stroke: sign of a pontine tegmentum lesion.

Pure hemisensory syndrome can be caused by small strokes occurring in a number of regions, including the thalamus and pons. Differentiation of the pontine sensory syndrome from the thalamic sensory syndrome has generally been made on the basis of distribution of sensory loss and involvement of specific sensory modalities but not without uncertainties and difficulties. Because the pontine tegmentum plays a pivotal role in generating horizontal eye movement, we attempted to discriminate these 2 syndromes by analyzing horizontal eye movements in stroke patients with pure hemisensory syndrome. Horizontal saccade, pursuit, vestibulo-ocular reflex (VOR), and VOR cancellation (VORC) were evaluated using electro-oculography in 6 patients with hemisensory syndromes, 3 due to pontine stroke and 3 due to thalamic stroke, and all were verified by MRI or CT. In addition, somatosensory evoked potentials (SEPs) were recorded. Smooth pursuit and VORC directed toward the side of the lesion were impaired unilaterally in patients with pontine sensory stroke, whereas those 2 movements were intact bilaterally in patients with thalamic sensory stroke. Saccade and VOR were preserved in all patients. SEPs were normal in all patients with pontine and thalamic sensory strokes. No difference was found in the pattern of sensory disturbance between the 2 types of stroke patients. Ipsilateral impairment of the smooth pursuit system may be a sign of a pontine lesion in patients with hemisensory stroke.

Long latency responses in pure sensory stroke due to thalamic infarction.

Our study was designed to clarify the role of the thalamus in the generation of the electrically elicited long-latency reflexes (LLR) in voluntarily activated hand muscles. EMG responses of the thenar muscles were evoked by electrical stimulation of the median nerve at the wrist at motor threshold intensity in 10 patients with acute pure sensory stroke due to thalamic infarction. Concomitant recording of somatosensory evoked potentials (SEPs) was performed. The subjects were asked to steadily abduct the thumb at 20-30% of maximal force against a force transducer. Rectified and averaged EMG activities were recorded. The LLR II was missing completely or significantly attenuated in the majority of the patients (9 of 10), of whom 3 also had delayed latency. Abnormal SEPs were documented in 7 patients (7 of 10). In the follow-up, 5 patients had partial reversal of LLR II. LLR II was still pathological in 1 fully recovered patient. Our results further confirm the transcortical generation of LLR II and imply that a thalamic relay is present in the afferent limb of the LLR.

Clinical-radiologic correlations in pure sensory stroke.

Clinical-radiologic correlations in 27 patients with pure sensory strokes (PSS) were retrospectively studied. Dysesthesias from pontine lesions were more severe than those from thalamic lesions. Pontine PSS but not thalamic PSS selectively affected vibration and position sense, leaving pinprick and temperature perceptions intact. Thalamic lesions but not pontine tended to spare the trunk.

Pure or predominant sensory stroke due to brain stem lesion.

Pure or predominant hemisensory symptoms can be seen in patients with brain stem stroke. However, there have been no reports in which sufficient numbers of patients were studied with detailed descriptions on the sensory patterns and imaging findings. We describe 17 patients presenting with pure or predominant hemisensory symptoms due to brain stem stroke in whom CT scan and/or MRI identified appropriate lesions. Eleven patients had an infarct and 6 had a hemorrhage. Aside from sensory deficit, the majority had dizziness and gait ataxia. Fifteen patients had paramedian dorsal pontine lesions associated with pure or predominant lemniscal sensory involvement, often in the cheiro-oral (n = 4) or leg dominance (n = 4) patterns. The lesions of the former group tended to be located more medially compared with those of other patients, which is in agreement with the sensory topography of the pontine lemniscal sensory tract. Bilateral facial or perioral sensory symptoms were noted in 6 patients. One patient with a dorsolateral pontine lesion had selective spinothalamic modality impairment, while one with a lateral midbrain infarct had sensory deficit of all modalities. Pure or predominant brain stem sensory stroke is most often produced by small infarcts or hemorrhages in the paramedian dorsal pontine area and may be differentiated from thalamic pure sensory stroke by the following characteristics: frequent association of dizziness/gait ataxia, predominant lemniscal sensory symptoms, occasional leg dominance or cheiro-oral pattern, and frequent bilateral perioral involvement.

5-16-01 Cutaneous reflexes in patients with pure motor or pure sensory stroke

5-16-01 Cutaneous reflexes in patients with pure motor or pure sensory stroke

Long-term Prognosis of First-Ever Lacunar Strokes

Information concerning the long-term prognosis of lacunar strokes is still limited and has shown different results. The aim of this study was to investigate the long-term prognosis of first-ever lacunar strokes and the possible role of clinical prognostic factors and different pathogenic mechanisms. Between March 1990 and November 1993, a cohort of consecutive patients presenting with first-ever lacunar infarcts was prospectively evaluated after stroke onset at day 0 to 3 and/or day 7, every 3 months up to 1 year, and every 6 months thereafter. All patients were studied according to a protocol that included demographic and clinical data, neurological examination, Toronto Stroke Scale, Barthel Index, Rankin Scale, CT scan, routine laboratory workup, electrocardiogram, carotid duplex scanning, and echocardiogram. More recently, patients have also been evaluated with transcranial Doppler ultrasonography. Recurrent strokes, myocardial infarction, and death were registered through direct observation, chart review, or interviews with the attending physician or family members. One hundred forty-five patients-94 (65%) with pure hemiparesis, 33 (23%) with sensorimotor stroke, 11 (8%) with ataxic hemiparesis, 5 (3%) with pure sensory stroke, and 2(1%) with dysarthria-clumsy hand syndrome-were followed for a median period of 39 months. During follow-up ther were 17 deaths (3 vascular), 30 recurrent strokes (1 fatal), and 4 myocardial infarctions. Five-year survival rate free of recurrent stroke was 63% (95% confidence interval [CI], 52% to 73%), while 5-year survival rate was 86% (95% CI, 78% to 91%). Cox proportional hazards analysis showed that age (p=.02) was the only significant predictor of survival free of recurrent stroke. Age (P<.001) and the degree of neurological dysfunction and functional disability at 7 days after the index stroke measured by the Toronto Stroke Scale (P=.05) and a Barthel Index score <40 (P=.04) were the only significant predictors of death. The 5-year probability rate of stroke-free recurrence was 72% (95% CI, 60% to 81%). Sixty-three percent of the first recurrent strokes were lacunar infarcts. When clinical, laboratory, and CT data as well as possible etiopathogenic mechanisms of lacunar strokes were considered, Cox proportional hazards analysis could not identify any predictor of stroke recurrence. Our study confirms that lacunar infarcts are associated with low stroke recurrence and mortality rates. In our series, the majority of first recurrent strokes were also lacunar infarcts. Age, degree of neurological dysfunction, and functional disability at day 7 after the index stroke were significant predictors of death.

Sensory symptoms and signs and results of quantitative sensory thermal testing in patients with lacunar infarct syndromes.

Quantitative data on sensory impairment in stroke patients are limited. We measured the perception thresholds for temperature and thermal pain in patients with different lacunar syndromes, correlated the results with clinical and magnetic resonance imaging (MRI) findings, and studied the long-term prognosis of sensory dysfunction. Quantitative thermal testing was performed by means of the Marstock method in 39 patients with lacunar syndromes (pure motor, sensorimotor, or pure sensory stroke) and MRI findings compatible with occlusion of a single perforating artery. Thresholds for cold, warmth, and heat pain were obtained bilaterally from the cheek, hand, and leg. The unaffected side was used as control. Follow-up included clinical assessments and repeated quantitative thermal testing (in 17 patients) up to 1 year after stroke onset. Patients with pure sensory stroke and sensorimotor stroke (n = 22) had a significant thermal hypoesthesia on the affected side for all modalities and test locations. Patients with pure motor stroke (n = 17) exhibited thermal hypoesthesia for cold and heat pain in the hand and for cold perception in the leg. On MRI, infarcts causing pure motor and sensorimotor stroke were predominantly lenticulocapsular, while a thalamic site of infarction was found in pure sensory stroke. The prognosis of sensory impairment was favorable, except for poststroke pain syndromes in three patients. Quantitative thermal testing confirmed an involvement of spinothalamic pathways in lacunar infarcts causing pure sensory and sensorimotor stroke and revealed a subclinical sensory impairment in patients with pure motor stroke. Infarction sites were similar in patients with pure motor and sensorimotor stroke.

Long-term prognosis of symptomatic lacunar infarcts. A hospital-based study.

This study concerns the long-term prognosis of lacunar infarcts. We report the analysis of our hospital-based series of 178 patients consecutively admitted for a lacunar syndrome due to a lacunar infarct diagnosed with computed tomography and magnetic resonance imaging. Demographic data, medical history, vascular risk factors, and imaging data were recorded for each patient. The follow-up was 35 +/- 22 months. The lacunar syndrome was pure motor hemiparesis in 69 patients (39%), ataxic hemiparesis in 45 patients (25.4%), pure sensory stroke in 15 patients (8.5%), sensorimotor stroke in 14 patients (7.9%), and miscellaneous syndrome in 34 patients (19.2%). The 4-year survival rate was 80 +/- 4% and the 4-year survival rate without recurrent stroke was 85 +/- 3.5%. Using Cox proportional-hazards analysis, the predictors of death were age (P < .02), diabetes mellitus (P < .05), and cigarette smoking (P < .05). We did not find any predictors of recurrence. After 1 year, 74% of the patients had mild or no disability. Using logistic regression analysis, the predictive factors of disability were age more than 70 years (P < .01), diabetes (P < .01), history of stroke or transient ischemic attack (P < .05), and type of lacunar syndrome (P < .01). Imaging data, number of lacunes, and presence of leukoaraiosis were not predictors of outcome. Our study suggests that with a high survival rate, a low recurrence rate, and a relatively good functional recovery, lacunar infarcts have a relatively favorable prognosis.

Small primary intracerebral hemorrhage. Clinical presentation of 28 cases.

Although there have been sporadic reports of patients with small intracerebral hemorrhages presenting with discrete clinical features, the clinical and distributional characteristics of these hemorrhages have not been adequately investigated. We studied 28 patients who had primary intracerebral hemorrhage of a longest diameter < or = 1.5 cm as seen in computed tomographic scan and/or magnetic resonance imaging. Small primary intracerebral hemorrhages were found in the basal ganglia in 8 patients (2 with intraventricular hemorrhage), the posterior limb of the internal capsule in 8, the area of the fourth ventricle of the cerebellum in 7 (5 with intraventricular hemorrhage), the pontine tegmentum in 4, and the thalamomesencephalic area in 1. All patients except 3 were hypertensive, suggesting that most of the hemorrhages may have occurred because of rupture of small end arteries secondary to long-standing hypertension. Depending on their location, the hemorrhages clinically manifested as pure motor stroke in 7, pure sensory stroke in 6, vertigo/ataxia in 7, sensorimotor stroke in 4, and ataxic hemiparesis in 2 patients. One patient with thalamomesencephalic hemorrhage showed vertical gaze disturbance, and 1 with basal ganglionic hemorrhage presented with symptoms of acute hydrocephalus secondary to a relatively large amount of intraventricular hemorrhage. The prognosis of small intracerebral hemorrhage was generally excellent except for when patients were very old or when there was a significant amount of intraventricular bleeding. Small primary intracerebral hemorrhage has its predilection sites: basal ganglia, posterior limb of the internal capsule, area of the fourth ventricle of the cerebellum, and pontine tegmentum. Most of the hemorrhages are probably caused by rupturing of the small end arteries in the setting of chronic hypertension. They produce discrete clinical syndromes often mimicking classic lacunar syndrome, of which pure sensory stroke is relatively common.

Pure sensory stroke revealing a complex malformation of extra- and intracranial cerebral arteries

Pure sensory strokes (PSS) are usually due to thalamic lacunar infarcts. We report a case of PSS in a 34-year-old female suffering from migraine who complained of sudden isolated left-sided paresthesia involving face, upper and lower limbs. We found a complex vascular abnormality associating internal carotid artery occlusion, posterior cerebral artery agenesia, aneurysm at the posterior face of the carotid siphon and angiomatous rete at the top of the basilar artery. The acquired origin of the carotid artery occlusion by possible neonatal dissection is probable since this patient has a permeable carotid canal on CT scan.

Sensory syndromes in parietal stroke.

We studied 20 patients with an acute parietal stroke with hemisensory disturbances but no visual field deficit and no or only slight motor weakness, without thalamic involvement on CT or MRI and found three main sensory syndromes. (1) The pseudothalamic sensory syndrome consists of a faciobrachiocrural impairment of elementary sensation (touch, pain, temperature, vibration). All patients have an inferior-anterior parietal stroke involving the parietal operculum, posterior insula, and, in all but one patient, underlying white matter. (2) The cortical sensory syndrome consists of an isolated loss of discriminative sensation (stereognosis, graphesthesia, position sense) involving one or two parts of the body. These patients show a superior-posterior parietal stroke. (3) The atypical sensory syndrome consists of a sensory loss involving all modalities of sensation in a partial distribution. Parietal lesions of different topography are responsible for this clinical picture, which probably represents a minor variant of the two previous sensory syndromes. Neuropsychological dysfunction was present in 17 patients. The only constant association was between conduction aphasia and right-sided pseudothalamic sensory deficit. We conclude that parietal stroke can cause different sensory syndromes depending on the topography of the underlying lesion. Sensory deficits can be monosymptomatic but never present as a "pure sensory stroke" involving face, arm, leg, and trunk together.

Infarcts with a cardiac source of embolism in the NINDS Stroke Data Bank

To gain insight into neurologic signs relevant to the diagnosis of cardiogenic embolism, we analyzed data from 1,290 patients with cerebral infarcts in the NINDS Stroke Data Bank. Based solely on the presence of potential cardiac sources of embolism, we divided patients into groups of high (N = 250), medium (N = 167), and low (N = 873) risk of a cardiogenic mechanism for their stroke. Diminished level of consciousness was highly associated with the presence of a cardiac source of embolism. Of the four primarily cortical deficits assessed, three (visual field abnormalities, neglect, and aphasia) showed a highly significant graded relationship to the cardiac risk groups. For the fourth cortical deficit (other nonlanguage cognitive functions), this relationship did not attain statistical significance. Conversely, hemiparesis without sensory or cortical deficits had a strong inverse association to the presence of a cardiac source of embolism. This inverse association was weaker for sensorimotor strokes and nonexistent for pure sensory strokes. Although some neurologic findings had highly significant associations with the presence of a cardiac source of embolism, their predictive value for an embolic source was low.

Etiology of motor or sensory stroke: A prospective study of the predictive value of clinical and radiological features

The diagnostic utility of clinical and radiological features for distinguishing penetrating artery disease from other causes of stroke has been questioned. To address this issue, we prospectively evaluated more than 40 features in 85 patients with pure motor, sensorimotor, or pure sensory syndromes. Nonischemic causes were present in 4 patients. The causes of ischemic stroke in the other 81 patients were penetrating artery disease (32 patients), large artery occlusive disease (17), cardioembolism (12), other causes (8), and undetermined (12). Of the features evaluated, frequent transient ischemic attacks (greater than or equal to 1/day), transient ischemic attacks occurring only within 1 week of stroke, pure motor hemiparesis (similar involvement of face, arm, and leg), pure sensory stroke, and round or oval infarction were associated (p less than 0.05) with penetrating artery disease. However, only pure sensory stroke involving two or more regions of the body and pure motor hemiparesis associated with subcortical infarction of less than 1.5 cm had positive predictive values exceeding 90% for penetrating artery disease. Carotid bruit ipsilateral to an anterior circulation infarction, monoparesis, and striatocapsular infarction had positive predictive values exceeding 90% for causes other than penetrating artery disease; however, half of the striatocapsular infarctions were of undetermined cause. These data suggest that certain clinical and radiological features are useful for distinguishing penetrating artery disease from other causes of stroke.

Pure sensory stroke due to midbrain haemorrhage.

Pure sensory stroke due to midbrain haemorrhage.

Ｐｕｒｅ ｓｅｎｓｏｒｙ ｓｔｒｏｋｅを呈した延髄のｌａｃｕｎａｒ ｉｎｆａｒｃｔ

Pure sensory strokeを呈した延髄のlacunar infarctをMRIにて描出しえた1例を報告する.症例は58歳男性で, 右半身のしびれ感を主訴にて来院した.神経学的検査では顔面を除く右半身の温痛覚の低下を認めた.その他の神経脱落症状は認めなかった.CTスキャンでは明らかな異常を描出しえなかったが, MRIにて延髄の左辺縁すなわち左外側脊髄視床路にほぼ一致する部位にlacunar infarctを確認した.

A Lenticulocapsular Lacune Producing Pure Sensory Stroke

A 46-year-old Korean man is reported who developed a right-sided pure sensory stroke. Magnetic resonance images identified a small, left-sided lentiform lacune which abutted on the lateral portion of

Prospective study of lacunar infarction using magnetic resonance imaging.

Using computed tomography and magnetic resonance imaging, we prospectively studied 100 patients hospitalized with a lacunar infarct. Our aim was to evaluate the capabilities of magnetic resonance imaging in the detection and delineation of lacunes in a project of clinicotopographic correlations. Seventy-nine patients had a classic lacunar syndrome; 35 had pure motor stroke, 26 had ataxic hemiparesis, seven had sensorimotor stroke, and 11 had pure sensory stroke. A miscellaneous group of 21 patients had less typical lacunar syndromes, primarily with brainstem signs and symptoms. Among a total of 153 lacunes, magnetic resonance imaging detected at least one lacune appropriate to the symptoms in 89 patients. In 16 patients at least two lesions correlated with the clinical features, and precise clinicotopographic correlations were possible in 68 patients. Magnetic resonance imaging was more effective when it was performed a few days after the stroke. Lesions causing different types of lacunar syndromes had significantly different volumes, suggesting that the size of the lesion may influence clinical features. Magnetic resonance imaging may be the imaging technique of choice in the study of lacunar syndromes.

Lacunar Infarctions and Dysarthria

To the Editor. —Patients with extensive ischemic cortical strokes in the middle cerebral artery territory usually experience aphasia when the dominant cerebral hemisphere is lesioned, and dysarthria when the nondominant hemisphere is involved. 1 Lacunar infarctions are small, deep ischemic strokes (with an average lesional diameter of less than 20 mm). 2,3 In such cases, aphasia is unusual. Some patients with either right or left hemispheric lacunar infarctions present with dysarthria, but little is known about that symptom. 4 To study the location of the lesions responsible for dysarthria in lacunar infarctions and the associated neurologic symptomatology, we performed a clinical examination and computed tomography of the head in 227 consecutive patients with lacunar infarctions (125 pure motor hemiparesis; 42 pure sensory stroke; 34 sensorimotor stroke; 7 ataxic hemiparesis, 4 dysarthria-clumsy hand; and 15 atypical lacunar syndromes). Analysis of the results showed dysarthria in 24.5% of patients (56 cases). The mean