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PubMed2002

Silent brain infarction in patients with rheumatic mitral stenosis.

Silent brain infarction (SBI) is defined as asymptomatic infarction areas detected in computerized tomography (CT) scans in patients without a history of stroke. The incidence of SBI is increased in CT or magnetic resonance imaging in patients with carotid stenosis and with atrial fibrillation (AF), but its relation with rheumatic mitral stenosis (MS), another major source of emboli, is uncertain. The aim of this study was to investigate the incidence of SBI in patients with MS. Fifty-three patients with MS (44 females and 9 males; range 25-52 years; mean age 38 +/- 7 years) diagnosed by transthoracic echocardiography (TTE) were enrolled in the study. Mitral valve calcification, left atrium (LA) dimension, and the presence of associating mitral regurgitation on TTE were recorded. Electrocardiographic evaluation was done for rhythm analysis and neurologic examination was performed prior to cerebral CT. Carotid artery Doppler examination was carried out in patients with SBI to exclude carotid artery lesions. Patients with a history of hypertension, diabetes mellitus, anticoagulant drug usage, presence of thrombus in LA, left ventricular segmental or systolic dysfunction, or other valve diseases were excluded from the study. The incidence of SBI was found to be 24.5% in patients with MS (47% cortical, 53% lacunar). SBI was observed to be significantly high in patients with LA dimension > 4 cm or in patients with AF (p < 0.05). The SBI incidence was markedly higher if AF was found with enlarged LA when compared with patients having sinus rhythm and small LA (p < 0.01). When moderate to severe mitral regurgitation was associated with MS, the SBI incidence was found to be lower (p < 0.05). Although SBI was higher in patients with MVA < 1.5 cm2, it was not statistically significant (p > 0.05). No significant correlation was found between calcific and noncalcific valves for SBI (p > 0.05). Our data suggest that SBI may be expected in about 1/4 of patients with MS. The presence of LA enlargement and AF increase the incidence of SBI in patients with MS, whereas the presence of moderate to severe mitral regurgitation decreases the incidence of SBI.

Adult↗
PubMed2005

Clinical significance of detection of multiple acute brain infarcts on diffusion weighted magnetic resonance imaging.

BACKGROUND: Detection of multiple acute brain infarcts (MABI) by diffusion weighted magnetic resonance imaging (DWI) may provide information about stroke mechanism in (1) acute lacunar stroke, where evidence of MABI suggests a cause other than small artery disease (SAD), such as embolism or vasculitis (type 1 MABI); or (2) acute non-lacunar stroke, where MABI in the territory of at least two of the aortic branches supplying the brain indicates the presence of aortic or cardiac embolism rather than artery to artery embolism (type 2 MABI). OBJECTIVE: To evaluate the prevalence of MABI and their impact on aetiological classification and prevention of stroke in patients with acute ischaemic stroke examined with DWI. METHODS: 182 consecutive patients defined by DWI were evaluated. Stroke aetiology was classified according to the TOAST criteria, though "lacunar stroke" included patients with possible aetiologies other than SAD. RESULTS: Type 1 MABI were detected in 21/72 patients (29%) with lacunar stroke, and type 2 MABI in 8/110 (7%) with non-lacunar stroke. A possible stroke mechanism different from SAD was found in nine type 1 MABI cases (43%): cardiac embolism (4); other determined aetiology (3); aortic embolism (2). Cardiac (2) or aortic (1) sources of embolism were detected in eight type 2 MABI cases. MABI patients with cardiac or aortic sources of embolism were treated with warfarin, the remainder with aspirin. CONCLUSIONS: Detection of type 1 MABI in patients with lacunar stroke improved diagnostic confidence and the choice of antithrombotic treatment. Further study is needed on stroke prevention in MABI cases caused by SAD alone.

Brain↗
PubMed1976

[Demonstration total brain infarct with radioisotope angiography].

In the field of organ transplantation and in brain death patients where intensive-care measures may seem superfluous, the demonstration of cessation of cerebral blood flow by X-ray angiography is generally agreed to be the diagnostic procedure of choice to prove irreversible loss of cerebral function. There are, however, certain drawbacks involved in X-ray angiography. Arterial puncture is necessary. Furthermore, the procedure can be time-consuming, thus making the continuation of adequate intensive-care measures more difficult. At the same time the circulatory condition may worsen causing hypoxic damage to the organ to be transplanted. In the present paper, the authors report on 13 patients with clinical signs of brain death where cessation of cerebral blood flow was demonstrated atraumatically by intravenous radioisotope angiography (RIA) using a multicrystal gammacamera (Baird Atomic) and the bolus-injection technique with 99m Tc-pertechnetate. Nine patients had severe brain injuries, 2 patients had brain tumours, 1 patient had encephalitis and 1 patient had suffered prepartal thrombosis of the sinus sagittalis. In all patients EEG recordings were isoelectric. At the time when the RIA was performed systolic blood pressure had decreased to 62-85 mmHg (x = 71 mmHg), while body temperature had declined to 31-36,5 degrees C (x = 34 degrees). According to the present results, which were all confirmed by subsequent bilateral carotid X-ray angiography, total brain infarction is unequivocal when the following criteria are satisfied using RIA: 1. when the radioisotope bolus flows along the common carotid arteries but does not proceed any further than to the base of the skull or around the scalp structures, 2. when, at the moment when the radioactivity outlines the scalp structures, neither the intracranial arteries nor the capillary bed or the venous sinuses are visible, 3. when the time-activity curves across the hemispheres show simply a plateau of low count rate without the activity peak typical for cerebral tracer circulation and 4. when the activity peak, typical for venous outflow, is missing from the time-activity curves for the cervical areas. In 12 patients with extremely reduced cerebral blood flow it was demonstrated that the RIA findings were clearly different from those obtained at brain death. Moreover, not one of 438 other patients undergoing RIA exhibited the same features which were associated with brain death. The authors conclude that RIA involves the same degree of safety as X-ray angiography in the diagnosis of total brain infarction but is superior to the latter when the diagnostic procedure has to be performed quickly, thus reducing the risk of any further damage to a prospective donor organ.

Adolescent↗
PubMed2001

[Objective evaluation of visual field loss in a patient with branch retinal artery occlusion and brain infarction].

PURPOSE: To evaluate visual field loss using multifocal ERG(m-ERG), multifocal VEP(m-VEP), and Heidelberg Retina Flowmeter(HRF) in a patient with branch retinal artery occlusion(BRAO) and brain infarction. CASE: A 38-year-old man noticed inferior-nasal visual field loss in the left eye, and was referred to Keio University Hospital. He suffered from paralysis in the left leg due to brain infarction at the age of 24. However, he had not noticed visual field loss due to the brain infarction. His left fundus showed retinal edema in the area of a superior-temporal retinal artery occulusion. He was diagnosed as having BRAO. The Goldmann and Humphry perimetric examinations revealed homonymous quadrantanopia in the upper left field as well as inferior visual field defect in the left eye. RESULTS: Both m-ERG and m-VEP, especially second-kernel responses, were reduced in the affected retinal area of BRAO. But only m-VEP was affected in the corresponding area of homonymous quadrantanopia in the upper left field. The retinal flow in the area with BRAO evaluated by HRF was decreased in some areas and not in others, suggesting that retinal function was not necessarily consistent with retinal circulation. CONCLUSIONS: m-ERG and m-VEP are useful To differentiate retinal lesions from brain lesions in visual field loss.

Adult↗
PubMed2003

Cortical laminar necrosis in brain infarcts: serial MRI.

High-signal cortical lesions are observed on T1-weighted images in cases of brain infarct. Histological examination has demonstrated these to be "cortical laminar necrosis", without haemorrhage or calcification. We report serial MRI in this condition in 12 patients with brain infarcts. We looked at high-signal lesions on T1-weighted images, chronological changes in signal intensity and contrast enhancement. High-signal cortical lesions began to appear about 2 weeks after the ictus, were prominent at 1-2 months, then became less evident, but occasionally remained for up to 1.5 years. They gave high signal or were isointense on T2-weighted images and did not give low signal at any stage. Contrast enhancement of these lesions was prominent at 1-2 months, and less apparent from 3 months, but was seen up to 5 months.

Adult↗
PubMed1985

Effect of dexamethasone on serum protein extravasation in experimental brain infarcts of monkey: an immunohistochemical study.

Experimental brain infarcts were produced in 12 adult baboons (Papio cynocephalus) by transorbital permanent clipping of the left middle cerebral artery. One group (seven monkeys) received daily injections of 1 mg/kg dexamethasone, starting 1 h after vascular occlusion and continuing till the end of the experiment. Another group (five monkeys) was not treated. One week after vascular occlusion the volume of infarcts and peri-infarct edema was estimated morphometrically on histological sections, using Masson's trichrome stain and the peroxidase-anti-peroxidase (PAP) technique for visualization of serum protein extravasation. In the untreated animals the average volume of infarct was 6.57 +/- 4.23% (mean +/- SD) and the volume of edema 7.83 +/- 2.93% of ipsilateral hemisphere. In the treated animals the infarct volume was not different (7.95 +/- 3.00%), but the volume of peri-infarct edema was significantly lower (2.82 +/- 3.06%, p less than 0.05). The results obtained indicate that dexamethasone treatment reduces the development of peri-infarct edema but does not influence the size of infarcts.

Animals↗
PubMed2001

Cerebral blood flow and metabolism in silent brain infarction and related cerebrovascular disorders.

The appropriate management of silent stroke requires better understanding of the haemodynamic status in the brain. However, only a few studies have examined cerebral blood flow and metabolism in subjects with silent stroke. Positron emission tomography demonstrated a slight decrease in cortical blood flow with an increase in oxygen extraction fraction (ie misery perfusion) in subjects with silent brain infarction, whereas both cerebral blood flow and oxygen metabolism decreased in patients with symptomatic brain infarction (matched hypoperfusion). These findings confirm that brain circulation is haemodynamically compromised in subjects with silent stroke. Another important point is that subcortical silent stroke may induce a reduction in cortical blood flow and metabolism by a disconnection mechanism (ie diaschisis) between the cortex and the subcortical structures. Silent infarction is not innocuous in terms of compromised cerebral circulation, which may lead to cognitive decline or subsequent clinical stroke. In the future, further developments in functional imaging will permit a more sophisticated analysis of brain circulation and metabolism in silent stroke.

Brain↗
PubMed1989

Adenylate kinase enzyme activity in cases of brain infarction.

The adenylate kinase (AK) enzyme activity in plasma and CSF of acute brain infarctions was examined. The normal values of enzyme activity in plasma reached from 1.7-5.6 U/l, and in CSF from 0.23-0.71 U/l. According to this present classification a significant CSF increase in AK activity was found with semi-severe and severe brain infarctions. With the CCT an increased enzyme activity was shown with infarction in or close to the cortex. In no case was an alteration of AK activity in the serum sample. CSF samples showing blood contamination or pleocytosis led to false pathological results with examination of AK activity.

Acute Disease↗
PubMed1995

[The pathogenesis of brain infarction in the posterior cerebral artery territory].

In order to clarify the etiology of brain infarction in the posterior cerebral artery (PCA) territory, we investigated 85 patients (29 women and 56 men, mean age: 63.6 years old) with PCA territory infarction confirmed by computed tomography or magnetic resonance imaging. Patients with thalamic infarction alone were excluded from the present study. Cerebral angiography was performed in 72 subjects. The diagnosis of the mechanism of brain infarction was made on the basis of cerebral angiographic and echocardiographic (presence of cardiac disease as a potential embolic source) findings. Embolism was inferred when the presence of the patent PCA ipsilateral to the infarction, reopening of the occluded PCA or intraluminal filling defect was demonstrated by angiographic studies. In addition, we divided these patients into three groups according to potential source of emboli; cardiogenic, atherothrombotic (so-called artery-to-artery embolism) and embolism of undetermined origin. We diagnosed the patient to have thrombotic mechanism, when an occlusion of the PCA was demonstrated without presence of an embolic source (heart diseases or stenotic arterial lesions proximal to the occluded PCA). When the mechanism (embolic or thrombotic) could not be clearly distinguished, we categorized them "unclassified". When other apparent mechanisms such as arterial dissection, moyamoya disease etc, were demonstrated, we classified them in "miscellaneous". According to the above criteria, 50 patients (59%) were diagnosed as having embolism, only two patients (2%) had definite thrombosis, 28 patients (33%) "unclassified", and five patients (6%) "miscellaneous" (2 arterial dissection, 1 radiation vasculopathy, 1 migraine, 1 moyamoya disease).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Aphasia owing to subcortical brain infarcts in childhood.

The aim of this study was to further define the clinical features of subcortical aphasia in children with deep brain infarcts and to define the sequelae associated with childhood strokes. We retrospectively studied nine children with left subcortical brain infarcts who presented with acquired language disorder and underwent language investigations based on standardized tests. Stroke in these patients involved the left internal capsule, lenticular or thalamic nuclei, or a combination of these. Early aphasic manifestations following the deep cerebral infarcts affected language expression. These included mutism, nonfluent speech, word finding difficulties, and phonemic and semantic paraphasia. Speech comprehension was generally more preserved. All patients subsequently improved, although variably; sequelae such as dysfluency, word finding difficulties, and written language learning impairment could be detected through standardized tests in six of them (all younger than 6 years at the time of the infarct). Two of the three remaining patients (both older than 6 years at the time of the infarct) had a full recovery. Our study confirms the concept of childhood subcortical aphasia, depicts the linguistic profile in these patients, and sustains the indication of systematic formal language assessment during the follow-up of all children with subcortical infarct involving the dominant hemisphere.

Adolescent↗
PubMed2001

Scattered brain infarct pattern on diffusion-weighted magnetic resonance imaging in patients with acute ischemic stroke.

BACKGROUND AND PURPOSE: Infarct patterns on brain imaging contribute to the etiologic classification of ischemic stroke. However, the association of specific subtypes of infarcts and etiologic mechanisms is often weak, and acute lesions are frequently missed on initial computed tomography (CT). Diffusion-weighted imaging (DWI) is superior in visualizing acute ischemic lesions as compared to CT and conventional magnetic resonance imaging (MRI). In our prospective study, we addressed the question whether a distinct pattern of infarction on DWI is associated with infarct etiology and clinical outcome. METHODS: Sixty-two patients with clinical signs of acute ischemic stroke and negative acute CT upon admission underwent DWI within 10 days after the ictus. Neurological status was documented using the NIH stroke scale. A scattered lesion pattern was defined by at least 2 separate hyperintense DWI lesions within the territory of one of the major cerebral arteries. Ischemic lesions were defined as acute if the region was demarcated strongly hyperintense in all DW images, and if the apparent diffusion coefficient was below normal. RESULTS: In 32 patients, DWI revealed a scattered lesion pattern, while in 30 patients a single acute lesion was detected. In patients with scattered lesions, potential arterial or cardiac embolic sources were detected in 26 patients (81.3%), as compared to 5 patients (16.6%) in the group with single lesions (chi(2) test, p < 0.0001). The neurological status of patients with scattered lesions improved significantly more than among patients with single lesions (Mann-Whitney test, p < 0.0003). CONCLUSION: A scattered lesion pattern on DWI in patients with acute brain infarction and negative initial CT scan is associated with an embolic etiology and may indicate a favorable clinical outcome.

Adult↗
PubMed2006

Insular involvement in brain infarction increases risk for cardiac arrhythmia and death.

OBJECTIVE: Brain injuries may induce cardiac dysrhythmias and sudden cardiac death. METHODS: We analyzed 12-lead electrocardiograms of 493 consecutive patients with brain infarction (BI) proved by an magnetic resonance imaging and 493 control subjects matched for age, sex, and center. Insular involvement (insula (+/-)) was assessed by two independent readings of the magnetic resonance imaging scans. Cases were followed for 5 years. RESULTS: Acute BI was independently associated with heart rate (< or = 64 beats/min), abnormal repolarization, atrial fibrillation, and ventricular and supraventricular ectopic beats. Lower heart rate in BI patients was due to an interaction with smoking (p for interaction = 0.004). Insula(+) group was significantly associated with abnormal repolarization with no interaction with infarct side. Atrial fibrillation by history was also more frequent in the insula(+) than in the insula(-) group (p = 0.07). After adjustment for age, sex, cardiovascular history, and handicap at admission, right insula(+) BI was significantly associated with 2-year all-cause death (hazard ratio, 2.11; 95% confidence interval, 1.27-3.52) and with vascular death (hazard ratio, 2.00; 95% confidence interval, 1.00-3.93). In multivariate analysis including age, sex, cardiovascular history, handicap at admission, and lesion side, increased QTc interval and left bundle branch block were independent predictors of all-cause and vascular mortality at 2 years in right insula(+) patients. INTERPRETATION: These findings support the notion that right insular involvement may lead to electrocardiographic abnormalities with potential prognostic implications. This could be important for optimal care in patients with right insular infarct.

Adult↗
PubMed1994

Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke. Relationship with index-stroke subtype, vascular risk factors, and mortality.

BACKGROUND AND PURPOSE: We wanted to establish independent associations of various clinical variables, computed tomographic (CT) scan features, presenting stroke subtypes, and outcome with the presence of silent infarcts on CT. METHODS: We studied 755 consecutive patients in a prospective registration of patients with first-ever supratentorial atherothrombotic, cardioembolic, or lacunar stroke or stroke of undetermined cause by multiple logistic regression analysis. RESULTS: Two hundred six patients (27%) with a first symptomatic territorial or small deep ischemic stroke had one or more silent infarcts on CT. Of all silent lesions, 169 (82%) were small and deep. Silent infarcts were significantly more strongly associated with a lacunar than atherothrombotic (odds ratio [OR], 1.59; 95% confidence interval [CI], 1.02 to 2.47; P = .039) or cardioembolic (OR, 1.89; 95% CI, 1.2 to 2.99; P = .005) index stroke. Silent territorial lesions were more strongly associated with cardioembolic than with lacunar stroke but not with atherothrombotic stroke. In this respect, no differences were found between the atherothrombotic and undetermined-cause group. Advanced age and hypertension were the only risk factors that were significantly associated with silent infarcts (OR, 1.76; 95% CI, 1.14 to 2.71; P = .011; and OR, 1.58; 95% CI, 1.13 to 2.21; P = .007; respectively), mainly because of a strong independent association of these risk factors with silent small deep infarcts (OR, 1.75; 95% CI, 1.10 to 2.79; P = .018; and OR, 1.57; 95% CI, 1.09 to 2.24; P = .014; respectively). A cardioembolic source or atrial fibrillation in specific was not independently associated with any type or number of silent infarcts. Significant carotid stenosis (diameter reduction > 50%) was not significantly associated with any type of silent lesion. Initial severe handicap (Rankin Scale score > 3), 30-day case fatality rate, and 1-year mortality were not affected by the presence of silent infarcts. CONCLUSIONS: The strong association of silent small deep lesions with first symptomatic small deep infarcts suggests a common underlying mechanism (presumably small-vessel vasculopathy), whereas cardiogenic embolism and large-vessel thromboembolism are the most likely causes in both silent and first symptomatic territorial infarcts. Single or multiple silent infarcts do not predict a cardioembolic stroke mechanism in first symptomatic supratentorial brain infarcts. As silent infarcts do not predict the cause of carotid embolic stroke in first symptomatic brain infarcts, their presence should not influence the decision on carotid surgery. Silent infarcts do not affect the degree of initial handicap, 30-day case fatality, or 1-year mortality. The significance of silent infarcts for predicting possible future cognitive decline and risk of recurrent stroke deserves further study.

Adult↗
PubMed2000

Brain infarcts due to scorpion stings in children: MRI.

We report two children with severe neurological complications after having been stung by a scorpion. Clinical and MRI findings suggested brain infarcts. The lesions seen were in pons in one child and the right hemisphere in the other. The latter also showed possible hyperemia in the infarcted area. No vascular occlusions were observed and we therefore think the brain infarcts were a consequence of the scorpion sting. The cause of the infarct may be hypotension, shock or depressed left ventricular function, all of which are frequent in severe poisoning by scorpion sting.

Animals↗
PubMed1993

Silent brain infarctions in patients with first-ever stroke. A community-based study in Umbria, Italy.

BACKGROUND AND PURPOSE: The relative frequency of computed tomographic evidence of old cerebral infarctions without prior history of stroke, and their effect on short- and long-term outcome of patients with first-ever ischemic stroke, are currently unknown. Silent infarctions may relate to specific risk factors and may influence the rate of survival free of handicap. METHODS: We studied the prevalence of such lesions in patients registered with SEPIVAC, a community-based survey of stroke incidence and outcome in the Sixth Local Health Unit of Umbria, Italy. Of 375 first-ever strokes, 209 patients with cerebral infarction (computed tomogram done within 30 days after the stroke) were included in this study. Computed tomograms were reviewed blindly, and cases were classified as having a single lesion or multiple lesions; in the latter case, it was assumed that at least one silent brain infarction was present. The two groups were compared in terms of risk factors and outcome. To avoid a selection bias, these patients were also compared with 68 patients who were not submitted to computed tomography but were judged on clinical grounds to have a > 90% probability of having suffered a cerebral infarction. RESULTS: Risk factors and outcome did not differ between patients without and with a computed tomogram. In the latter group, 80 patients (38.3%; 95% confidence interval, 31.7%-44.9%) had silent brain infarction. Male sex (odds ratio, 1.84; 95% confidence interval, 1-3.4), ischemic changes on an electrocardiogram (odds ratio, 2.5; 95% confidence interval, 1.3-4.9), and--in the multivariate analysis--hypertension (odds ratio, 1.46; 95% confidence interval, 1.1-2) were significantly more frequent in these patients. Outcome at 1, 6, and 12 months was not influenced by the presence of silent infarctions. CONCLUSIONS: This community-based study shows that silent brain infarctions in patients with first-ever stroke are not significantly related to risk factors commonly described in hospital-based series (atrial fibrillation, transient ischemic attack, etc.); rather, silent infarctions seem to be a marker of widespread vascular disease.

Aged↗
PubMed1993

Suppressed sympathetic skin response in brain infarction.

BACKGROUND AND PURPOSE: Autonomic failure is known to manifest commonly in stroke, but very little attention has been given to various features of sympathetic dysfunction such as sudomotor dysregulation in cerebrovascular diseases. In the present study, our purpose was to assess quantitatively sympathetic reflex activity in brain infarction by measuring the sympathetic skin response. METHODS: We recorded the sympathetic skin response to electric and auditory stimulations simultaneously on both hands in 58 patients with brain infarction and in 36 healthy control subjects. RESULTS: The response amplitudes were significantly decreased and the latencies prolonged in both hemispheral (n = 49) and brain stem (n = 9) infarctions compared with the control subjects. The amplitudes were diminished in both the acute and late phases of infarction, but the latencies were prolonged only in the acute phase. CONCLUSIONS: Sympathetic dysfunction in brain infarction seems to be much more extensive than has previously been thought. In the present study, we have demonstrated impaired sympathetic skin responses, reflecting definite suppression of the reflex activity of the sympathetic nervous system.

Acoustic Stimulation↗
PubMed1990

[Brain infarcts in humans during middle age and senility. I. Defects of blood-brain barrier permeability in immunocytochemical studies].

Brains of the deceased in the age from 45 to 57 years (6 cases) and from 80 to 101 years (9 cases) with ischemic brain damage were studied. Technique of the peroxidase-antiperoxidase (Sterberger et al. 1970) was used for visualization of the brain tissue reactivity for albumin, IgG, alpha 1-antitrypsin and alpha 2-macroglobulin. In all cases the disturbances of the blood vessels permeability were found. The BBB deterioration within the first days of brain infarct seems to be smaller in senile age than in middle age. However, after some days senile blood vessels permeability increases and become similar in both age groups.

Aged↗
PubMed1999

Masticatory force and function in patients with hemispheric brain infarction and hemiplegia.

Recent functional animal studies have reported that the motor control of masticatory muscle function is bilaterally guided by both hemispheres, which may fundamentally differ from the cortical control of limb muscle function. In this study, we investigated whether unilateral cortical brain infarction induces different impairments in masticatory and upper limb motor performance. Evidence of the importance of both hemispheres in controlling masticatory movements would be greater if the masticatory function were shown to be unimpaired in patients with severe hemiplegia. The masticatory function of 16 patients with severe hemiparesis caused by brain infarction in the region of the middle cerebral artery was studied by means of interview, clinical examination, and bite-force measurements. Finger-thumb grip-force measurements and clinical examination of the upper limbs were also performed for evaluation of the effect of infarction on upper limb motor function. Localization of the infarction was confirmed with computer tomography and magnetic resonance imaging. The Scandinavian Stroke Scale demonstrated that each patient had a major unilateral cortical infarction which had caused a marked handicap with a serious impairment of upper limb function on the contralateral side. The clinical examination revealed no major signs of temporomandibular disorders, and the masticatory muscles, when examined by palpation, contracted symmetrically. None of the patients with unilateral brain infarction showed any differences in bite forces between the healthy and paralyzed sides. These results indicate that, in hemiparetic patients, great differences may exist between the motor performances of the masticatory and upper limb muscles. The present investigation clinically illustrates the importance of both hemispheres in the control of masticatory function and movements.

Adult↗