Pure Motor Hemiparesis Research Articles

A longitudinal fMRI study: in recovering and then in clinically stable sub-cortical stroke patients

The aim of this 1-year longitudinal fMRI study was to compare hand motor activation patterns between cerebrovascular paretic patients with a subcortical infarction and healthy elderly subjects and to evaluate the changes between the subacute phase and the chronic phase of recovery. We studied eight right-handed patients with pure motor hemiparesis due to a single ischemic infarct of the corticospinal tract. Each patient underwent a first fMRI (E1) 20 ± 9 days after stroke, a second (E2) after 4 months and a third (E3) 12 months after stroke. During each fMRI session, the patients performed an active motor task consisting of audio-paced (1 Hz) finger flexion–extension of the paretic hand and underwent a passive motor task consisting of flexion–extension of the paretic hand performed by an examiner. Data were analyzed with SPM99 (random effect analyses). Patients had recovered at E2, were stable between E2 and E3, but still experienced a hand weakness. Displacement of activation maxima coordinates in patients compared to healthy subjects suggested an early reorganization within the SMA and a secondary reorganization within the ipsilesional S1M1 at E2. The main differences between patients and healthy subjects were (1) recruitment of the posterior part of the cingulate cortex and SMA, (2) a general hyperactivation (except in the deefferented primary motor cortex) and (3) an evolution in the S1M1 activation from an early (20 days after stroke) contralesional hyperactivation to a later (4 months after stroke) ipsilesional hyperactivation concomitant to recovery. Changes in activation were confirmed by the passive task that involved no effort and little attention. Despite clinical stability, changes in brain processing seemed to occur between E2 and E3 corresponding to a normalization of ipsilesional S1M1 activation, a decrease of bilateral cerebellar activation, and a progressive increase in SII-BA 40 activity suggesting evolving compensatory networks to sustain recovery.

New Concepts in Lacunar Stroke Etiology: The Constellation of Small-Vessel Arterial Disease

Objective: To update the less frequent etiologies causing lacunar infarcts (LIs). To highlight recent advances in risk factors, clinical syndromes, topography, complementary tests and long-term prognosis in this subtype of ischemic stroke. Patients and Methods: The most important studies are analyzed, from CM Fisher works, selecting those referring to LIs of unusual etiology, and recent advances and controversies in the clinical management of LI are discussed. Results: LIs are found in approximately 11% of patients admitted with stroke. The pure motor hemiparesis (55%) constitutes the most usual lacunar syndrome. However, lacunar syndromes may not be caused by LIs in 10–20% of cases. LIs caused by microembolism and cholesterol embolism from the aortic arch are reviewed. Hematological diseases can also cause LI, such as polycythemia rubra vera, essential thrombocythemia and primary antiphospholipidic antibody syndrome. Other etiologies are carotid plaque embolism, severe stenosis of a perforated arteriole and amyloid angiopathy. Infectious arteritis by neurolues, neurocysticercosis, neuroborreliosis, by AIDS or Helicobacter pylori infection have also been associated with the presence of LIs. Likewise, inflammatory arteritis in systemic lupus erythematosus or granulomatous angiitis, cocaine abuse and panarteritis nodosa have been related to LI, although in the latter LI would be caused by a thrombotic microangiopathy and not by vasculitis. Conclusions: LI is an ischemic stroke subtype with a characteristic clinical presentation and a short-term favorable prognosis. Although high blood pressure constitutes the main risk factor and the main etiology, LIs may be caused, in less than 5% of cases, by various etiologies, mainly hematological diseases and infectious or inflammatory arteritis. It is essential to make a correct etiological diagnosis for LI as treatment will be different according to its etiology.

Etiology and Long-Term Prognosis of Unilateral Paramedian Pontine Infarction with Progressive Symptoms

Progressive pure motor hemiparesis is a common feature in paramedian pontine infarction. To assess the etiology, clinical course and long-term prognosis of this stroke subtype, we identified 26 patients with progressive symptoms in a retrospective study, treated in our hospital between 1993 and 1998. All patients had more than one stroke risk factor, and in 20, basilar branch disease, an atherosclerotic occlusion of basilar perforating arteries, was causative. Most patients developed severe hemiparesis after a mean time of 3 days, nearly 50% showed deterioration in connection with a fall in systolic blood pressure. The patients were followed up for 4–9 years: 4 patients had further strokes, 5 died, and 17 patients were independent, which may be interpreted as a good long-term prognosis.

Differential Impairment of Individuated Finger Movements in Humans After Damage to the Motor Cortex or the Corticospinal Tract

The purpose of this study was to quantify the long-term loss of independent finger movements in humans with lesions relatively restricted to motor cortex or corticospinal tract. We questioned whether damage to the motor cortex or corticospinal tract would permanently affect the ability to move each finger to the same degree or would affect some fingers more than others. People with pure motor hemiparesis due to ischemic cerebrovascular accident were used as our experimental sample. Pure motor hemiparetic and control subjects were tested for their ability to make cyclic flexion/extension movements of each finger independently. We recorded their finger joint motion using an instrumented glove. The fingers of control subjects and of the unaffected hands (ipsilateral to the lesion) of hemiparetic subjects moved relatively independently. The fingers of the affected hands (contralateral to the lesion) of hemiparetic subjects were differentially impaired in their ability to make independent finger movements. The independence of the thumb was normal; the independence of the index finger was slightly impaired, while the independence of the middle, ring, and little fingers was substantially impaired. The differential long-term effects of motor cortical or corticospinal damage on finger independence may result from rehabilitative training emphasizing tasks requiring independent thumb and index movements, and from a greater ability of the spared components of the neuromuscular system to control the thumb independently compared with the other four fingers.

Patients with capsular infarct and Wallerian degeneration show persistent regional premotor cortex activation on functional magnetic resonance imaging

Background and Purpose: By using neurorehabilitation outcome measures and functional magnetic resonance imaging (fMRI), we attempted to elucidate the effect of Wallerian degeneration (WD) in the pyramidal tract distal to a posterior capsular stroke on functional recovery. Methods: In 18 patients with pure motor hemiparesis caused by capsular infarct, we identified the presence of WD and then tested whether it affected the rate of motor improvement and the final motor outcome. The discharge T2-weighted MRI (139 ± 5 days on average after stroke) showed WD in 10 of 18 patients (WD-positive, n = 10; WD-negative, n = 8). All patients performed mass grasping of paretic fingers before and after inpatient neurorehabilitation for the fMRI. Results: Demographic characteristics, rate of disability change, final motor status, and volume of lesion were comparable between the groups. On the first fMRI, patterns of fMRI activation in the sensorimotor cortex, premotor cortex (PMC), and supplementary motor area were comparable. However, on the second fMRI, considerably more patients in the WD-positive group (8 out of 10) exhibited persistent contralateral activation in PMC than in the WD-negative group (1 out of 8; P =.0044, chi-square test). Ipsilateral PMC was also more frequently activated (P =.04) in WD-positive patients than in WD-negative patients. Conclusions: Persistent WD had no effect on the impairment or disability outcome; however, it was associated with novel regional activation on repeat fMRI after recovery. To determine whether persistent PMC activation resulted from effort or represents a general effect of WD on motor recovery will require a longer follow-up time and more precise control of functional measurement during imaging. Copyright © 2001 by National Stroke Association

Dysarthria in acute ischemic stroke: lesion topography, clinicoradiologic correlation, and etiology.

Although dysarthria is a frequent symptom in cerebral ischemia, there is little information on its anatomic specificity, spectrum of associated clinical characteristics, and etiologic mechanisms. An investigation of 68 consecutive patients with sudden onset of dysarthria due to a single infarction confirmed by MRI or CT was conducted. Dysarthria was associated with a classic lacunar stroke syndrome in 52.9% of patients. Isolated dysarthria and dysarthria-central facial and lingual paresis occurred in 2.9% (n = 2) and 10.3% (n = 7), respectively. Dysarthria-clumsy hand syndrome was observed in 11.7% (n = 8) of patients and associated with pure motor hemiparesis and/or ataxic hemiparesis in 27.9% (n = 19). The lesions were due to small-vessel disease in 52.9% (n = 36), to cardioembolism in 11.8% (n = 8), and to large-vessel disease in only 4.4% (n = 3) of cases. Infarctions were located in the lower part of the primary motor cortex (5.9%; n = 4), middle part of the centrum semiovale (23.5%; n = 16), genu and ventral part of the dorsal segment of the internal capsule (8.8%; n = 6), cerebral peduncle (1.5%; n = 1), base of the pons (30.9%; n = 21), and ventral pontomedullary junction (1.5%; n = 1). Isolated cerebellar infarctions affected the rostral paravermal region in the superior cerebellar artery territory. Extracerebellar infarcts causing dysarthria were located in all patients along the course of the pyramidal tract. This finding correlates with the frequent occurrence of associated pyramidal tract signs in 90.7% (n = 62) of patients. Isolated cerebellar infarcts leading to dysarthria were in all cases located in the territory of the superior cerebellar artery.

Abstracts of literature

Abstracts of literature

Hemorrhagic Lacunar Stroke

A total of 17 patients with lacunar syndromes due to intracerebral hemorrhage or hemorrhagic lacunar stroke (pure motor hemiparesis 9, sensorimotor stroke 5, pure sensory stroke 3) are reported. Data from these patients were obtained from consecutive stroke patients included in the prospective Hospital Sagrat Cor-Aliança Stroke Registry. Hemorrhagic lacunar stroke accounted for 3.8% of all cases of lacunar syndrome (n = 439) and 7.4% of all cases of intracerebral hemorrhage (n = 229) entered in the database. Demographic, anamnestic, clinical and neuroimaging variables in patients with hemorrhagic lacunar stroke, non-lacunar intracerebral hemorrhage and non-hemorrhagic lacunar stroke were compared. Predictors of hemorrhagic lacunar stroke were assessed by logistic regression analysis. Hypertension, cigarette smoking and involvement of the internal capsule were significantly more frequent in patients with hemorrhagic lacunar stroke than in those with non-lacunar intracerebral hemorrhage, whereas nausea and vomiting, altered consciousness, speech disturbances, hemianopia, and ventricular hemorrhage were significantly less frequent. As compared with non-hemorrhagic lacunar stroke, patients with hemorrhagic lacunar stroke were more likely to have hypertension, sudden stroke onset (minutes), head injury, headache, and basal ganglia involvement and less likely to have diabetes, gradual stroke onset (hours), and dysarthria. After multivariate analysis, only headache (OR 10.14), sudden onset (OR 9.89), and dysarthria (OR 0.10) were independent predictors of hemorrhagic lacunar stroke. Accordingly, the presence of headache and sudden onset of symptoms and absence of dysarthria may be useful signs for distinguishing hemorrhagic lacunar stroke from other causes of lacunar stroke.

Abstracts of literature

Abstracts of literature

Wallerian degeneration of the pyramidal tract does not affect stroke rehabilitation outcome.

To test whether Wallerian degeneration (WD) of the pyramidal tract as signaled by MRI affects rehabilitation outcome in patients with subcortical infarction (internal capsule or corona radiata). Recent radiologic evidence suggests that WD occurs no earlier than 3 months after a subcortical infarction. A total of 77 consecutive patients with pure motor hemiparesis due to an initial subcortical infarction were assessed on admission and discharge with the Functional Independence Measure (FIM) for disability and Stroke Impairment Assessment Set (SIAS, full = 25) for impairment. WD was defined by a high-intensity area detected along the pyramidal tract below the level of lesion on T2-weighted MR image (WD+). Age, sex, side of stroke, Mini-Mental State Examination score, and volume of lesion were comparable for each group. Length of stay (LOS) was significantly longer (p < 0.05) in WD+ (130 days) than in WD- (105 days). There was no difference in the change of FIM (WD+, 99 to 111; WD-, 95 to 107) or SIAS measures (WD+, 12 to 16; WD-, 13 to 16) made on admission and discharge, nor was there any effect of the timing of the rehabilitation experience (< or = 90 days or >90 days after stroke). After stroke, apparent WD of the pyramidal tract may slow functional recovery but does not limit final rehabilitation outcome of pure motor hemiparesis. Study of the mechanisms of compensation for this delayed pyramidal tract degeneration will enhance the scientific basis for rehabilitation.

Testing the validity of the lacunar hypothesis: the Northern Manhattan Stroke Study experience.

Few studies have attempted to validate the "lacunar hypothesis." The accuracy of identifying lacunar and other nonlacunar mechanisms of infarction will be increasingly important in evaluating potential stroke treatments. The aim of this study was to determine the value of lacunar syndromes in predicting radiologic lacunes and the value of clinicoradiologic lacunes in predicting "lacunar infarction" as final stroke mechanism. From 1990 to 1994, 591 patients with cerebral infarction, who were from northern Manhattan and over the age of 39, were prospectively examined. Data were collected on the admitting clinical syndrome (lacunar or nonlacunar) and brain imaging findings. Lacunar syndromes were categorized as pure motor hemiparesis (PMH), pure sensory syndrome (PSS), sensorimotor syndrome (SMS), ataxic-hemiparesis (A-H), and other lacunar syndromes. Brain imaging findings were classified as radiologic lacune or nonlacune. Positive predictive values, sensitivities, and specificities of lacunar syndromes for identifying radiologic lacunes were calculated. The final mechanism of infarction was determined after review of all the diagnostic tests and compared among the lacunar groups. Lacunar syndromes occurred in 225 cases. PMH was the most common lacunar syndrome, accounting for 45%, SMS 20%, A-H 18%, and PSS 7%. Lacunar syndromes had an overall positive predictive value (PPV) of 87% for detecting radiologic lacune: PSS 100%, A-H 95%, SMS 87%, and PMH 79%. Among the 195 patients who presented with a lacunar syndrome and had this condition confirmed radiologically, 147 were classified as having a final diagnosis of lacunar mechanism of infarction (PPV = 75%). Atherosclerosis accounted for 17 (9%), cardioembolism 10 (5%), cryptogenic 17 (9%), and other unusual causes 4 (2%). While lacunar syndromes, especially PSS and A-H, are highly predictive of lacune, in about one in four patients presenting with lacunar syndromes confirmed radiologically the condition is associated with nonlacunar mechanisms of infarction. Noninvasive neurovascular and cardiac evaluations are still warranted even among patients with lacunes.

Pure motor hemiparesis due to pontine infarction as the presenting sign of neurosyphilis

A 50‐year‐old man with minimal risk factors for cerebrovascular disease had a pure motor hemiparesis due to a pontine infarction. Syphilis serology and CSF findings indicated a previously unrecognized meningovascular syphilis as the cause of the stroke. At variance with the majority of recently reported cases, no prodromal syndrome preceded the cerebrovascular event, and there was no HIV coinfection. Treatment with erythromycin and minocycline was followed by clinical improvement and normalization of main CSF parameters including VDRL; oligoclonal bands and local IgG synthesis, however, were still detectable in post‐treatment CSF.

Posterior circulation infarcts simulating anterior circulation stroke. Perspective of the acute phase.

Ischemic stroke patients whose initial clinical presentation suggests an involvement of the anterior circulation (AC) are sometimes found to have a posterior circulation (PC) infarct, a fact that may generate erroneous decisions in clinical management. We investigated the prevalence of this misdiagnosis in the first few hours after stroke onset. We performed a cohort study of 158 patients hospitalized within 5 hours of onset of a presumed AC ischemic stroke, as diagnosed on clinical grounds. Final CT or pathology diagnosis was AC infarct in 128 patients (81%), a repeatedly negative CT in 14 (9%), PC infarct (5 pons, 1 midbrain and cerebellum, 6 supratentorial territory of the posterior cerebral artery) in 12 (8%), and other or undiagnosed lesions in 4 (3%). AC and PC stroke patients did not differ in terms of age, vascular risk factors, and initial severity, but the latter were more frequently men (83% versus 53%; P = .04), were hospitalized later (mean +/- SD, 168 +/- 86 versus 109 +/- 55 minutes; P = .001), and presented a pure motor hemiparesis or a sensorimotor stroke (50% versus 33%) more often than their counterparts. At baseline CT, PC stroke patients never exhibited an early parenchymal hypodensity in the carotid territory or a hyperdense middle cerebral artery, which were instead found in 59% (P = .0003) and 31% (P = .02) of AC stroke patients, respectively. Early neurological deterioration, 1 month case-fatality rate, and disablement in survivors were comparable in the two groups. Shortly after onset the clinical discrimination between AC and nontypical PC infarcts is not reliable, which explains the frequent occurrence of this misdiagnosis. Emergency CT scan helps in the differential diagnosis only when it demonstrates an early focal hypodensity within the carotid territory.

Pure motor hemiplegia including the face induced by an infarct of the medullary pyramid

Four autopsy cases of pure motor hemiparesis due to medullary pyramid infarcts have been previously reported. The deficits that were described included overt limb weakness and “slight facial weakness”. According to current neurological teaching, the lesion responsible for an upper motor neuron facial palsy affects the corticobulbar tract at the level of the midpons or more rostrally.

Syndromes of pontine base infarction. A clinical-radiological correlation study.

Although there have been sporadic reports of lacunar syndromes due to pontine base infarction, studies of clinical-radiological correlation in sufficient numbers of patients have not yet been reported. We studied the clinical features of 37 patients with acute infarcts that mainly involved the base of the pons and correlated the clinical syndromes with the radiological findings. The clinical presentations included pure motor hemiparesis (PMH) in 17, sensorimotor stroke in 3, ataxic hemiparesis (AH) in 4, and dysarthria-clumsy hand (DA-CH) syndrome in 6 patients. Variants of AH included 1 patient with dysarthria-hemiataxia and 2 with quadrataxic hemiparesis, and in 4 patients dysarthria-facial paresis syndrome was considered a variant of DA-CH syndrome. Hypertension was the single most common and important risk factor, and the pathogenetic mechanisms of ischemia were likely to be small arterial (lacunar) occlusion or basilar atheromatous branch occlusion in most of the patients. Our clinical-radiological correlation study suggested that large lesions involving the paramedian caudal or middle pons correlate with severe hemiparesis (PMH), whereas lesions of similar size located in the paramedian rostral pons tended to produce DA-CH syndrome. Lesions producing AH were located variously but tended to spare the pyramidal tracts. The prognosis of these patients is fair or good, although residual hemiparesis remained in patients with initially severe hemiparesis. Our data suggest that the various lacunar syndromes that follow pontine base infarcts reflect the balance of the involvement of the corticospinal, corticopontocerebellar, and corticobulbar tracts. Analysis of radiological findings aids in determining the clinical-anatomic correlation in patients with pontine base infarction.

Pure midbrain infarction

We studied 22 patients with first stroke and infarct limited to the midbrain on MRI. We selected these patients (8%) from 281 with posterior circulation infarct admitted consecutively into a primary care center. All patients underwent a systematic protocol of investigations including MR imaging and angiography, and echocardiography. Most infarcts fitted well to arterial territories drawn in preestablished templates. Middle midbrain involvement was the most common, mainly in the paramedian territory supplied by the basilar artery. Infarct in the mesencephalic territory of the posterior cerebral artery was less common, while superior cerebellar artery territory infarct was extremely rare, and posterior choroidal artery territory infarct did not occur. The neurologic picture was dominated by eye-movement disorders. Patients with isolated upper or lower midbrain infarct had no localizing clinical findings, but patients with middle midbrain infarct had a localizing picture mainly with nuclear or fascicular third nerve palsies that commonly developed in isolation. Vertical gaze paresis, pure motor hemiparesis, four-limb ataxia from unilateral lesion, and hypesthetic ataxic hemiparesis also occurred. Contrary to a common view, cardioembolism was not a more common etiology than basilar artery stenosis or small-vessel disease.

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.

Pure motor hemiparesis and sensorimotor stroke. Accuracy of very early clinical diagnosis of lacunar strokes.

Clinical differentiation of lacunar from nonlacunar strokes in the very early phase could help to exclude patients with lacunar stroke from pharmacologic trials designed for nonlacunar strokes, namely, those with thrombolytic agents. In a continuous series of acute ischemic stroke patients, we evaluated how accurately a clinical diagnosis of pure motor hemiparesis or sensorimotor stroke formulated in the first hours from onset predicts a lacunar stroke documented by cerebral computed tomography or by autopsy. We examined 517 patients (299 men, 218 women; mean +/- SD age, 67 +/- 10 years) within 12 hours (mean +/- SD, 6.1 +/- 3.2 hours) of the event. At hospital admission, we observed 151 (29%) patients with pure motor hemiparesis and 68 (13%) patients with sensorimotor stroke. Computed tomography or autopsy was compatible with a lacunar stroke (ie, detection of a lacune or permanently negative computed tomography) in 170 (33%) patients, of whom 123 (72%) had pure motor hemiparesis and 47 (28%) had sensorimotor stroke. This led to a sensitivity of 72%, a specificity of 72%, a positive predictive value of 56%, and a negative predictive value of 84%. Overall positive predictive value of pure motor hemiparesis was 58% (60% for two areas and 58% for three areas involved), and that of sensorimotor stroke was 51% (87% for two areas and 40% for three areas involved). By separately evaluating the sides of lesions, we found a positive predictive value of 46% for right-side infarcts and of 72% for left-side infarcts. Right-side lesions constituted 51% of lesions in lacunar syndrome patients with lacunar stroke, 76% in those with nonlacunar stroke, 19% in nonlacunar syndrome patients with lacunar stroke, and 31% in those with nonlacunar stroke (P < .0001). During the first days of hospital stay we observed a deterioration of 21% of lacunar syndrome patients with nonlacunar stroke and an improvement of 49% of nonlacunar syndrome patients with lacunar stroke, with appearance and disappearance of symptoms of cortical involvement, respectively. The examination of these patients after the occurrence of these clinical changes would have led to a daily increase of the positive predictive value up to a maximum of 66% at day 7. Pure motor hemiparesis and sensorimotor stroke diagnosed within 12 hours of the event are poorly predictive of lacunar strokes. Hence, the very early identification of these syndromes cannot be used for patient selection in therapeutic trials.

Neurologic improvement in pure motor hemiparesis: implications for clinical trials.

Knowledge of the natural history of certain stroke subtypes is essential for the proper analysis and interpretation of clinical trials of stroke therapy. We evaluated the degree of weakness on admission and again 7 to 10 days later in 62 patients with pure motor hemiparesis (PMH) and 280 patients with motor deficits from other stroke syndromes (OSS). During the 7-to-10-day study interval, we found that the OSS group worsened slightly in motor function, whereas the PMH group improved (p = 0.01). Among those who improved in both groups, those in the PMH group improved to a greater extent than did those in the OSS group (p = 0.02). This occurred despite a greater frequency of worsening during the first 12 hours after stroke onset in the PMH group. By the fourth day following PMH onset, a majority of patients had improved, and this improvement was sustained until day 10. The two groups did not differ significantly in age, race, sex, history of cardiac disease, hematocrit, anticoagulation treatment, blood glucose, or medical complications in hospital. Lacunar infarcts occurred in 84% of PMH and 23% of OSS. Patients with PMH show significant spontaneous improvement in weakness within 7 to 10 days of admission, compared with patients with OSS. Stratification by admission stroke syndrome in clinical trials may be necessary before judging the efficacy, or lack thereof, of a therapeutic agent.

Pure Motor Hemiparesis with Stable Somatosensory Evoked Potential Monitoring during Aneurysm Surgery

We report a patient who sought treatment for an acute subarachnoid hemorrhage as a result of an intracranial aneurysm. Management included early surgical repair and intraoperative monitoring of evoked potentials. Pan-angiography revealed berry aneurysms of the communicating anterior artery and right middle cerebral artery. Surgery was uneventful, and the somatosensory evoked potential monitoring did not show any abnormalities. Nevertheless, the patient showed a neurological deficit due to a clip-related infarct in the right middle cerebral artery territory characterized by a right hemiparesis with no sensory deficit. This case report supports the possibility of false-negative results in single-mode intraoperative monitoring during aneurysm surgery.