Parkinsonism in patients with cerebral infarcts

Reuck, Jacques De; Sieben, G.; Coster, W. De; Eecken, H. vander

doi:10.1016/0303-8467(80)90035-9

Cited by 29 publications

(24 citation statements)

References 9 publications

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“…Dodge et al 3 and Black et al 4 included CIs and hemorrhages, and their incidences were 12.5% and 10%, respectively. Holmes 5 and de Reuck et al 6 studied embolic and nonembolic CIs and noted incidences of 13.8% and 7.9%, respectively. Holmes 5 noted a higher incidence with embolic (23%) than with nonembolic (12.4%) CIs.…”

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confidence: 99%

Postinfarction seizures. A clinical study.

Gupta

Naheedy

Elias

et al. 1988

Stroke

184

125

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We retrospectively studied 90 patients with postinfarction seizures to determine the clinical features (onset, number, type), prognosis, and electroencephalographic and computed tomographic findings; we included infarctions of all etiologies. Thirty-three percent of the 90 seizures appeared early (within 2 weeks after the infarction), and 90% of the 30 early seizures appeared within 24 hours after the infarction. Seventy-three percent of the 90 seizures occurred within the first year, and only 2% occurred >2 years after the infarction. Fifty-six percent of the 90 seizures were single, and status epilepticus was seen in only 8%. Early-onset seizures were more likely to be partial (57% of 30); late-onset seizures were more likely to be generalized (65% of 60). Thirty-nine percent of the 90 initial seizures recurred, and there was no significant difference in recurrence rate between early-or late-onset initial seizures. Twenty-two percent of the 90 initial seizures became multiple recurrent seizures, and we could identify a precipitating factor in 86% of the 35 recurrent seizures. The most common electroencephalographic abnormality in the 61 patients so examined was focal slowing (61%), but recurrent seizures occurred in 100% of the four patients with periodic lateralized epileptiform discharges and in 75% of the eight patients with diffuse slowing. Computed tomography in 61 patients showed that large infarctions were associated with early (p<0.021) and multiple (/><0.05) seizures. Deep infarctions on computed tomograms (cortical infarctions extending to subcortical structures) tended to cause recurrent seizures (/><0.057). Seizures in 88% of the 90 patients could be managed with monotherapy.

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confidence: 99%

Postinfarction seizures. A clinical study.

Gupta

Naheedy

Elias

et al. 1988

Stroke

184

125

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“…Vascular parkinsonism (VP) may manifest as a combination of extrapyramidal symptoms, resembling Parkinson disease (PD), but VP has not been clearly defined, 14) so the reported frequency of VP after cerebral infarction varies from 2% to 38%. 1,12,18) MR imaging of patients with VP found more subcortical lesions than in patients with PD or hypertension, and identified two types of VP: acute onset of lesions located in the subcortical gray nuclei, and an insidious onset with lesions diffusely distributed in the white matter. 22) Investigation of the clinical and neuropathologic characteristics of VP in autopsy cases found most VP patients had widespread lesions in the frontal white matter and relatively slight lesion in the basal ganglia, suggesting that VP might be related to frontal white matter lesions.…”

Section: Resultsmentioning

confidence: 99%

“…In this study, 57% of patients showed extrapyramidal signs, a considerably higher rate compared to the previous studies. 1,12,18) The present population included only patients with mild or no neurological deficit, in contrast to the previous studies, which included patients with severe deficit. Severe neurological impairment may conceal extrapyramidal signs, so the population difference can explain the higher rate in this study.…”

Section: Resultsmentioning

confidence: 99%

Long-Term Follow Up of Patients With Good Outcome After Intra-arterial Thrombolysis for Major Arterial Occlusion in the Carotid Territory: Clinical and Magnetic Resonance Imaging Evaluation

Sorimachi¹,

Ito

Morita³

et al. 2010

Neurol. Med. Chir.(Tokyo)

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Long-term clinical symptoms, including extrapyramidal signs, and magnetic resonance (MR) imaging studies were retrospectively analyzed in 21 patients with good outcome (modified Rankin scale scores 0-2) after successful recanalization of occluded major arteries by intra-arterial thrombolysis with mechanical disruption. Changes in high intensity areas (HIAs) and cerebral atrophy in the ischemic hemisphere were evaluated on follow-up fluid-attenuated inversion recovery MR images. Extrapyramidal signs, short-stepped gait and/or masked face, were observed in 12 of 21 patients during the follow-up period (11 to 68 months, mean 42 months). Enlargement of HIA was demonstrated in 10 of 18 patients undergoing follow-up MR imaging. Cerebral atrophy in the ischemic hemisphere was revealed on the follow-up MR images in all 18 patients. In nine patients with small infarctions, 20 ml or less on computed tomography scans, cerebral atrophy progressed more rapidly in four patients with extrapyramidal signs compared to the other five patients without extrapyramidal signs (p º 0.05). More than half of the patients with good outcome showed extrapyramidal signs. Extrapyramidal signs in patients with small infarction may indicate rapid progression of cerebral atrophy. The occurrence of extrapyramidal signs might be related to delayed neuronal death in atrophic areas.

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“…Experimental and human autopsy studies have demonstrated that dopaminergic nerve terminals [11], GABA/substance P neurons (which give rise to the indirect pathway [62]) [12], dopamine receptors [13]and nicotinic acetylcholine receptors [14]in the striatum are highly vulnerable to ischemia, which may result in an increased susceptibility to parkinsonism. Damage to the white matter is also associated with parkinsonism [8, 9, 10, 15, 16, 17, 18], which has been assumed to be due to disconnection involving the extrapyramidal motor system [18]. These studies suggest that vascular parkinsonism (VP) is one of the secondary parkinsonisms of extranigral etiology [19, 20], in which the striatum and white matter are the main focuses in the pathogenesis of parkinsonism.…”

Section: Introductionmentioning

confidence: 99%

“…In 1929, Critchley [1]designated such cases as ‘arteriosclerotic parkinsonism’, reporting its clinical characteristics as compared to idiopathic Parkinson’s disease (IPD) consisting of rapid progression, symmetrical symptoms, absence of tremor and plastic rigidity instead of cogwheel rigidity. While he related the symptoms to vascular changes in the globus pallidus and, to a lesser extent, the substantia nigra, later autopsy- or neuroimaging-based studies have related parkinsonism to symmetrical vascular lesions in the putamen [2, 3, 4, 5, 6, 7]or cerebral white matter [8, 9, 10]. Experimental and human autopsy studies have demonstrated that dopaminergic nerve terminals [11], GABA/substance P neurons (which give rise to the indirect pathway [62]) [12], dopamine receptors [13]and nicotinic acetylcholine receptors [14]in the striatum are highly vulnerable to ischemia, which may result in an increased susceptibility to parkinsonism.…”

Section: Introductionmentioning

confidence: 99%

Symptomatic Characteristics of Parkinsonism and the Width of Substantia nigra pars compacta on MRI According to Ischemic Changes in the Putamen and Cerebral White Matter: Implications for the Diagnosis of Vascular Parkinsonism

Tohgi

Takahashi²,

Abe³

et al. 2001

Eur Neurol

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To investigate the significance of vascular lesions as a cause of secondary parkinsonism, we analyzed the symptomatic characteristics, the width of the substantia nigra pars compacta (SNpc) on MRI and the responsiveness to L-dopa in 227 parkinsonian cases, excluding those with drug-induced parkinsonism and neurodegenerative diseases other than idiopathic Parkinson’s disease (IPD). They were classified into those without a significant infarct in the basal ganglia (n = 144), those with status lacunaris in the putamen (SLP; n = 66) and those with confluent white matter hyperintensity signals (CWMH; n = 17). The 4- to 6-Hz tremor and cogwheel rigidity were significantly more frequent in cases without significant infarct (69%) than those with SLP (50%) and those with CWMH (12%; p < 0.05). Among cases with 4- to 6-Hz tremor and cogwheel rigidity, the frequency of patients with a reduced SNpc width and L-dopa responders did not significantly differ between those with SLP (73 and 83%, respectively) and those without significant infarct (83 and 86%, respectively), suggesting that the diagnosis for most of these cases would be probable IPD. In contrast, among cases without 4- to 6-Hz tremor and cogwheel rigidity, those with a reduced SNpc width or L-dopa responders were significantly less frequent among cases with SLP (25 and 38%, respectively) than among those without significant infarct (75 and 71%, respectively; p < 0.05). Patients with neither 4- to 6-Hz tremor and cogwheel rigidity nor reduction in the SNpc width, for whom the probable diagnosis was vascular parkinsonism (VP), were significantly more frequent in cases with SLP (26%) and with CWMH (40%) than those without significant infarct (8%), accounting for 10.6% of the total parkinsonian cases. These findings suggest that parkinsonian cases with SLP or CWMH consist of not only cases with vascular-lesion-related VP but also IPD in which vascular lesions are not directly related to parkinsonism. Absence of 4- to 6-Hz tremor, cogwheel rigidity and the reduction in the SNpc width could be indicators for differentiating VP from IPD.

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Parkinsonism in patients with cerebral infarcts

Cited by 29 publications

References 9 publications

Postinfarction seizures. A clinical study.

Postinfarction seizures. A clinical study.

Long-Term Follow Up of Patients With Good Outcome After Intra-arterial Thrombolysis for Major Arterial Occlusion in the Carotid Territory: Clinical and Magnetic Resonance Imaging Evaluation

Symptomatic Characteristics of Parkinsonism and the Width of Substantia nigra pars compacta on MRI According to Ischemic Changes in the Putamen and Cerebral White Matter: Implications for the Diagnosis of Vascular Parkinsonism

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