Thank you for updating your details. Log In. Sign Up. Become a Gold Supporter and see no ads. Log in Sign up. Articles Cases Courses Quiz. About Recent Edits Go ad-free. Edit article. View revision history Report problem with Article. Citation, DOI and article data. Jones, J. Lentiform nucleus. Conclusions Acute lenticular infarction induces mainly hemiparesis but no movement disorder. Associated sensory deficits, aphasia, and hemineglect underline clinically the function of the lenticular nucleus in connection with the prefrontal, temporal, and parietal cortices.
Although pure internal capsule infarction has been well documented, 1 - 4 infarction limited to the putamen—globus pallidus is poorly recognized. Two clinical syndromes associated with lesions limited to the lenticular nucleus have been defined by Giroud et al 5 : 1 behavioral and cognitive disorders associated with infarcts within the globus pallidus and 2 motor disorders dystonia and cognitive disorders associated with disorders in the putamen.
Bhatia and Marsden 6 reviewed the behavioral and motor consequences of focal lesions of the basal ganglia in patients described in the literature with lesions of the lenticular and caudate nucleus and found that dystonia was the most frequent motor disorder and abulia, the most frequent behavioral disorder. Similarly, lesions involving the lentiform nucleus, particularly the putamen, caudate nucleus, thalamus, 7 , 8 and parietal cortex, 9 often in combination, have been associated with acute and subacute posthemiplegic focal dystonia or hemidystonia.
Other motor disorders, such as unilateral chorea, 11 hemichorea-hemiballism, asterixis, acute stereotypies, 12 acute focal dystonia, 13 and subacute parkinsonism, 14 have also been reported after unilateral lesions of the lentiform nucleus but often also involve the caudate nucleus or the internal capsule.
Lesions involving the globus pallidus may cause behavioral and speech disorders, 5 , 17 as well as motor disorders including delayed contralateral hemidystonia 10 or subacute choreoathetosis. To investigate acute, purely lenticular ischemic infarction, we selected and reviewed all cases of patients with such lesions in the Lausanne Stroke Registry.
Patients were selected from a collective of consecutive patients prospectively included in the Lausanne Stroke Registry between and Of consecutive patients with a first-ever symptomatic subcortical hemispheric stroke, had a lesion in the basal ganglia confirmed by computed tomography CT 93 [ We excluded all patients with hemorrhagic infarcts 5 [3.
Thirteen patients presented with infarcts involving the lenticular nucleus only; 12 of them had CT scans and 1 had MR imaging. These 13 patients form the basis for this study. All infarcts were in the territory of the perforating branches of the middle cerebral artery. The detailed investigations for patients included in the Lausanne Stroke Registry have been described elsewhere. Catheter angiography was performed in selected cases.
Blood tests consisted of blood cell count, hepatic and renal function tests, glucose level, total cholesterol level, sedimentation rate, VDRL, and tests of coagulation. Patients were divided into 2 groups according to the distribution of infarcts on neuroimaging scans. One group consisted of patients with infarcts limited to the putamen, while the second group consisted of patients with infarcts extending into the globus pallidus externus.
The criteria for cardiac sources of embolism included atrial fibrillation, sick-sinus syndrome, or a recognized source on echocardiography mural thrombus, wall akinesia or hypokinesia, endocarditis, aneurysm, prosthetic valves, or recent myocardial infarction.
Of the 13 patients 8 men and 5 women between 30 and 86 years of age with ischemic stroke limited to the lenticular nucleus, 9 patients had a lesion limited to the putamen and 4 patients had a lesion also involving the globus pallidus externus Table 1.
Six of the 13 patients had diabetes mellitus as a risk factor, 8 had arterial hypertension, 4 had hypercholesterolemia, 6 were smokers, and 3 had atrial fibrillation. Ten patients had diabetes mellitus or hypertension or both; 5 of them had no other source of infarction and had a lacunar stroke due to presumed small-artery disease. No patient had signs of middle cerebral artery stenosis or occlusion on transcranial Doppler ultrasonography, MR angiography, or conventional angiography.
A young woman, who was a smoker and used oral contraception, had no evidence of a definite cause. The ischemic lesion was 15 mm or larger in 5 patients with potential embolic sources large-artery disease in 3, cardioembolic sources in 2.
The lesions were smaller than 15 mm in 8 patients, 6 of whom had small-artery disease as the presumed cause of infarct. All patients had initial faciobrachiocrural motor hemisyndrome, but none showed parkinsonism or any abnormal movement during hospital stay or follow-up.
Of the 9 patients with a lesion limited to the putamen, 2 had moderate proportional ataxic faciobrachiocrural motor hemisyndrome, predominantly crural in 1.
There were 3 patients with proportional faciobrachiocrural motor deficit moderate in 2 and severe in 1 , with ataxia in the patient with a severe deficit and in 1 of those with a moderate motor hemisyndrome. All 3 patients had spinothalamic hemihypesthesia; it involved predominantly the upper limb in 1, associated with hemineglect, and the upper and lower limb in 2, associated with deep pain in the arm in 1 of the 2. Predominantly faciobrachial mild sensorimotor hemisyndrome with ataxia was present in 1 patient.
Three patients had moderate ataxic faciobrachiocrural motor hemisyndrome with ataxia predominating in the lower limbs, with spinothalamic sensory loss of the face in 2 and of the leg in another 1, associated with loss of postural sense and pallesthesia.
Four patients had a left-sided lesion involving the putamen and globus pallidus externus. Two right-handed patients had severe proportional faciobrachiocrural motor hemisyndrome with nonfluent aphasia, and 1 had moderate faciobrachiocrural motor hemisyndrome with ataxia.
One patient had a severe proportional faciobrachiocrural ataxic hemisyndrome with unilateral spinothalamic sensory loss in arm and leg. Ten patients recovered motor function well during the hospital stay, with complete recovery in 2 and persistence of discrete motor hemisyndrome in 8 with ataxia in 2.
All 10 patients were independent at home for their daily activities after hospitalization. Two patients remained disabled by a predominantly brachial hemiparesis. Word-finding difficulties persisted in both patients with initial nonfluent aphasia due to left putaminal-pallidal infarction. Hemisensory loss, hemineglect, and deep pain were always transient disorders, regressing during hospital stay.
All 13 patients had an ischemic lesion in the perforating branches of the middle cerebral artery. We found that acute unilateral infarction limited to the lenticular nucleus is rare 1.
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These are cookies intended to measure the audience: it allows to generate usage statistics useful for the improvement of the website. Verify now. Toggle navigation. Institutional subscriptions support Language. Keep me signed in. Forgot your password? Sign in with Facebook. Sign in with Apple. Description The lentiform nucleus is lateral to the caudate nucleus and thalamus, and is seen only in sections of the hemisphere.
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