Analysis of the reasons for exclusion from tPA therapy after early arrival in acute stroke patients.

OBJECTIVE: Only a small percentage of patients with acute stroke receive thrombolytic therapy, mainly due to late hospital arrival. Factors excluding those who arrive within 3h after stroke onset are less well known. PATIENTS AND METHODS: During the first year after implementing a protocol for stroke thrombolysis, we prospectively evaluated all patients with stroke admitted to our center within 3h from onset. Within-hospital time intervals were calculated and the reasons for exclusion from thrombolysis were analyzed. RESULTS: Ninety-six patients (representing 16% of all stroke patients admitted) arrived in less than 3h, and 25 of them (representing 7.5% of all patients with ischemic stroke) received thrombolytic therapy, with a door-to-needle interval of 51 min (range, 33-121). The reasons that accounted for 75% of therapy exclusions were non-modifiable (a too mild or improving deficit, and intracranial hemorrhage), except for a time window exceeded, which would probably require increasing public awareness about stroke. CONCLUSIONS: Most reasons for not applying thrombolysis to patients who arrive early enough are non-modifiable. Minimizing the door-to-needle time could compensate for late hospital arrival, which continues to be the main reason for not applying this therapy to stroke patients throughout the world.

Cardiac sympathetic denervation in symptomatic and asymptomatic carriers of the E46K mutation in the α synuclein gene.

OBJECTIVE: The aim of this study was to analyze autonomic function and cardiac sympathetic innervation in symptomatic and asymptomatic carriers of the E46K alpha-synuclein gene (SNCA) mutation. PATIENTS AND METHODS: Autonomic function tests were performed in six patients, four of whom were symptomatic carriers (ages: 46, 59, 52 and 28-years) and two who were asymptomatic carriers (ages: 52 and 29 years). Autopsy studies were performed on an additional two symptomatic carriers not eligible for autonomic testing. Patients completed the SCOPA autonomic questionnaire, and underwent the head-up tilt test accompanied by measurements of plasma norepinephrine. Valsalva maneuver and deep breathing tests, along with recording of sympathetic skin response (SSR) and cardiac MIBG scintigraphy were carried out. Myocardial tissue sections removed from the two autopsied cases were subjected to routine histological staining and immunohistochemical processing with monoclonal antibodies against tyrosine hydroxylase and alpha-synuclein. RESULTS: Both the four symptomatic and the older asymptomatic carriers reported abnormalities in the SCOPA questionnaire and had markedly diminished cardiac MIBG uptake. Plasma norepinephrine in the supine and tilted positions was normal in all subjects. Only one patient had significant orthostatic hypotension. There was a complete absence of tyrosine hydroxylase immunostaining in the myocardium of the two autopsied cases. INTERPRETATION: We have found imaging and histological evidence of cardiac sympathetic denervation in symptomatic and asymptomatic carriers of the E46K alpha-synuclein gene mutation. The sympathetic denervation appears to be organ-specific, with selective affectation of the heart given that plasma norepinephrine levels and blood pressure were normal.

Migraine-associated seizures with recurrent and reversible magnetic resonance imaging abnormalities.

Migraine and epilepsy are highly comorbid, but the nature of their association remains unclear. Exceptionally, reversible brain magnetic resonance imaging (MRI) abnormalities following migraine and seizures have been reported. There are no descriptions, however, of patients with recurrent brain MRI changes. We report a patient with repeated episodes of migraine-with-aura-associated seizures (migralepsy) and recurrent and reversible brain MRI abnormalities. Location of the abnormalities was always consistent with the neurologic deficits. The possibility that transient brain MRI abnormalities in a patient with migraine with aura followed by seizures may be due to migralepsy should be borne in mind to avoid misdiagnosis and potentially aggressive procedures.