Effect of nicardipine on somatosensory evoked potentials in patients with acute cerebral infarction.

Abstract

We evaluated the effect of nicardipine, a calcium channel blocker, on somatosensory evoked potentials (SEP) in 26 patients with acute cerebral infarction. Post treatment, 58% (15/26) of the N20 and P25 latencies were prolonged in the affected hemispheres; 8% (2/26) were shortened; and 35% (9/26) did not change. The mean N20 and P25 latencies were significantly prolonged two hours post treatment in the affected hemisphere (N20, P < 0-01, P25 P < 0O01). Nicardipine (Ni) had no effect on SEP components in the intact hemispheres. Needle electrodes were placed in Fpz, C3' and C4' (2 cm behind standard EEG C3 and C4), and the stimulating electrode was fixed to the skin over the median nerve at the wrist (electrode impedance 5 K). Stimuli were 0-2 ms square wave electrical pulses delivered with a frequency of 5 Hz and an intensity just above the thumb twitch threshold (current intensity 5-15 mA). The peak latencies of N20 and P25 components in the intact and affected hemispheres were recorded. At least three series of 256 responses were averaged for each side. The range of variability within individuals was less than 0 4 ms.All patients had SEP examinations and 12 patients had blood pressure (BP) measured (cuff method) before and two hours after they had one 40 mg oral dose of nicardipine. Measurements were carried out between 24 hours and seven days post-stroke ( The mean N20 and P25 latencies post-treatment were statistically significantly longer than pre-treatment in the affected hemispheres (N26 P < 0-01, P25 P < 0-01). There was no effect of nicardipine on SEP latencies in the intact hemispheres.2 Effect of nicardipine on BP (table 3) Two hours after receiving nicardipine, 75% of the 12 patients with hypertension had a decrease in BP. A statistically significant decrease in both systolic and diastolic pressures were observed.

Nicardipine: A Hypotensive Dihydropyridine-Type Calcium Antagonist with a Peculiar Cerebrovascular Profile

“…Similar to that observed for other drugs of the same family, the administration of nicardipine both orally (30-60 mg three times per day) or intravenously (3-10 mg/h) improved cerebral hemodynamics and neurologic examination performed three months after stroke (101)(102)(103). Objective measurements such as somatosensorial evoked potential (SEPs) and single-positron emission computerized tomography (SPECT) revealed, respectively, no effect of nicardipine on neuronal function in ischemic areas (104) and improvement of haemodynamics in ischemic regions in spite of hypotensive activity.…”

Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications

“…Neuronal Ca 2+ overload causes extensive cellular damage in ischemic stroke. Various Ca 2+ channel blockers (e.g., lercanidipine, nicardipine, cilnidipine) have protective effects on ischemic brains in animal models of ischemic stroke 385‐388 . Pertussis toxin, a G‐protein blocker, was also shown to protect against ischemic stroke by blocking Ca 2+ influx 389 …”

Nicardipine and Treatment of Cerebrovascular Diseases with Particular Reference to Hypertension-Related Disorders

“…Similarly as observed for other drugs of the same family, administration of nicardipine both orally (30-60 mg three times per day) or intravenously (3-1 0 mg/h) improved cerebral hemodynamics and neurologic examination performed 3 months after stroke (1 19-125). Objective measurements such as somatosensorial evoked potential (SEPs) and single positron emission computerised tomography (SPECT) revealed respectively no effect of nicardipine on neuronal function in ischemic areas (122) and improvement of haemodynamics in ischemic regions in spite of hypotensive activity (1 24). The main side-effect caused by nicardipine in stroke patients was hypotension which in some cases required to discontinue treatment (1 19) for avoiding the risk of cerebral hypoperfusion (1 25).…”