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Features, symptoms, and neurophysiological findings in stroke associated with hyperhomocysteinemia
S Evers1, H G Koch, K H Grotemeyer
1Department of Neurology, University of Münster, Germany. everss@uni.muenster.de
Insights
Hyperhomocysteinemia, an elevated homocysteine level, is a likely independent risk factor for stroke. Patients with hyperhomocysteinemia show distinct stroke patterns and impaired cognitive processing.
Area of Science:
- Neurology
- Vascular Medicine
- Biochemistry
Background:
- Hyperhomocysteinemia is a recognized risk factor for atherosclerosis and cerebrovascular disease.
- Elevated homocysteine levels are associated with increased risk of stroke, myocardial infarction, and peripheral vascular disease.
Purpose of the Study:
- To investigate clinical, biochemical, and neurophysiological differences in ischemic stroke patients with and without hyperhomocysteinemia.
- To determine the prevalence and impact of hyperhomocysteinemia on stroke characteristics.
Main Methods:
- A cohort of 125 stroke patients and 60 healthy controls were analyzed.
- Hyperhomocysteinemia was defined as total plasma homocysteine levels exceeding the mean plus 2 standard deviations of controls.
- Clinical data, biochemical markers, Doppler sonography, and event-related potentials were assessed.
Main Results:
- Twenty-seven percent of stroke patients had hyperhomocysteinemia.
- Hyperhomocysteinemia was associated with increased hypertension, uric acid, hematocrit, and microangiopathy.
- Patients with hyperhomocysteinemia exhibited prolonged P3 latency in event-related potentials, indicating cognitive processing impairment.
Conclusions:
- Hyperhomocysteinemia is a probable independent risk factor for stroke, present in approximately 20% of stroke patients.
- Hypertension and hyperuricemia may exacerbate stroke risk in individuals with hyperhomocysteinemia.
- Stroke patterns differ, with more cerebral microangiopathy lesions and cognitive processing deficits observed in hyperhomocysteinemic patients.
Background:
Hyperhomocysteinemia has been shown to be a mild independent risk factor for premature atherosclerosis, and there is evidence of an increased rate of peripheral vascular occlusive disease, myocardial infarction, and stroke.
Objective:
To evaluate clinical, biochemical, and neurophysiological findings in patients with ischemic stroke with and without hyperhomocysteinemia.
Subjects:
One hundred twenty-five consecutive patients with a history of stroke and 60 healthy control subjects.
Methods:
Patients were divided into those with and those without hyperhomocysteinemia, which was defined as blood levels beyond the mean total plasma homocysteine level plus 2 SDs of the healthy control group. History, symptoms, cause, patterns of infarction, biochemical data, continuous and transcranial Doppler sonography, and event-related potentials were recorded in all patients.
Results:
Twenty-seven patients had hyperhomocysteinemia. Compared with the 98 patients without hyperhomocysteinemia, they had an increased rate of hypertension (odds ratio, 3.5; 95% confidence interval, 1.0-12.6), an increased level of uric acid (P < .007), an increased hematocrit (P < .02), a higher rate of microangiopathy (odds ratio, 2.8; 95% confidence interval, 1.1-7.2), and a trend to a higher rate of multiple infarction. Furthermore, the P3 latency of the event-related potential was significantly increased in hyperhomocysteinemia (P < .004).
Conclusions:
Hyperhomocysteinemia is probably an independent risk factor for stroke, with a prevalence of about 20% in all patients with a history of stroke; however, additional factors (eg, hypertension, hyperuricemia) may have an enhancing effect. There are significant differences in stroke patterns between patients with and without hyperhomocysteinemia, with a higher rate of lesions typical of cerebral microangiopathy and a trend to multiple infarctions in the former. Impairment of cognitive processing as measured by visual event-related potential is more pronounced in hyperhomocysteinemia.