Biomedical subjects
Publications and source records attributed to Nazire Afsar.
A 43-year-old man with asystole and syncope occurring during cluster headache attacks is reported. The asystole and syncope attacks disappeared completely following prophylactic therapy with methysergide maleate. To the authors' knowledge, the present case is unique in associating asystole with cluster headache attacks and may be due to hyperactivity of the parasympathetic system.
BACKGROUND: Electrocardiographic changes are well known to appear with acute cerebrovascular events. OBJECTIVE: To investigate if QT dispersion (QTd) is increased in patients who have an acute stroke and if this increase could be related to lesion extent and/or localization. DESIGN: The study group consisted of 36 patients who had an acute stroke and no history or signs of cardiovascular disease. An age-matched control group (n = 19) free of cardiovascular disease was also included. Simultaneous 12-lead electrocardiograms (ECGs) were recorded within the first 24 hours (24h-ECG) and after 72 hours (72h-ECG) from stroke onset. QT dispersion was assessed both manually and automatically with assessors blinded to the clinical data. RESULTS: QT dispersion, corrected QTd, and automated QTd were significantly increased in the 24h-ECG compared with the 72h-ECG (60 [range, 20-80] milliseconds vs 40 [range, 0-80] milliseconds, P<.005; mean [SD], 56 [19] vs 36 [21] milliseconds, P<.001; and 50 [range, 14-94] vs 34 [range, 0-84] milliseconds, P<.005, respectively). However, QTd in the 72h-ECG was similar to QTd in the control group. While in the 24h-ECG corrected QTd was significantly greater in patients with large infarcts and large hemorrhages (mean [SD], 70 [20] vs 51 [20] milliseconds, P<.05), in the 72h-ECG corrected QTd was greater in patients with right vs left-sided lesions (mean [SD], 39 [18] vs 24 [18] milliseconds, P<.05). CONCLUSIONS: QT dispersion is increased in the first 24 hours in patients with acute stroke and no cardiovascular disease compared with the control group. Although this finding seems to be related to the size of the lesion rather than to the localization or type of stroke, after 72 hours specific lesion localization could also influence the QTd.
Even though stroke is known to be a common cause of status epilepticus (SE), the types of stroke or SE that may be associated are not yet clearly defined. The aims of this study were to assess the timing and type of SE in stroke patients and to observe the effects of stroke and the type of SE on the response to treatment and mortality. From May 1998 to May 2001 a total of 121 patients were admitted with SE. Among these, 30 cases (24.8%) of poststroke SE were identified and evaluated. There were 20 early-onset, and 10 late-onset SE. All stroke types were evenly distributed within the early-onset group, whereas only ischaemic stroke was found in the late-onset group. Posterior cerebral artery (PCA) infarcts were significantly more common within the latter (P: 0.0017). Nonconvulsive SE (NCS) was more frequent than convulsive SE (CS) in the early-onset group (P: 0.0352). There was a delay in the time-to-treatment for NCS compared to CS (P: 0.0007). Without, however any effect on the rate of response to first step treatment (intravenous diazepam and phenytoin; P: 0.6334). Thirteen patients died (43.3%) during hospitalisation. Disability was significantly associated with higher mortality in the early-onset group (P: 0.0201). As a conclusion, NCS seems to be an important issue in stroke, thus requiring a high degree of suspicion in an acute stroke setting to avoid further neuronal injury and morbidity.
OBJECTIVE: To determine the patterns of clinical presentation, lesion topography, and etiology in patients with ischemic stroke limited to the superficial territory of the posterior cerebral artery (s-PCA). METHODS: In the Lausanne Stroke Registry (LSR, 1983-1998), we determined the patterns of clinical presentation, lesion topography and mechanisms of stroke, among 117 patients with s-PCA infarction (s-PCAI) on brain imaging. RESULTS: s-PCAIs accounted for 30.5 % of all PCA territory ischemic strokes. The presumed etiology was embolism in 64 (54.5 %) patients [cardiac in 51 (43.5 %) and arterial in 13 (11 %)], indeterminate in 38 (32 %), PCA atherothrombosis in 4 (3.4 %), migraine in 4 (3.4 %), other rare causes in 4 (3.4 %), and multiple potential sources of embolism in 3 (2.5 %). The clinical findings were hemianopsia in 78 (67 %), quadrantanopsia in 26 (22 %), and bilateral visual field defects in 8 (7 %). Motor, sensory, or sensorimotor deficits were detected in 14 (12 %), 8 (6.8 %), or 8 (6.8 %) patients, respectively. Neuropsychological dysfunction included memory impairment in 20 (17.5 %; with left [L], right [R], or bilateral [B] lesions in 15, 2, or 3 patients, respectively), dysphasia in 17 (14.5 %; L/B: 14/3), dyslexia with dysgraphia in 5 (4 %; L/B: 4/1), dyslexia without dysgraphia in 10 (8.5 %; L/B: 8/2), hallucinations in 12 (10 %; L/R/B: 5/5/2), visual neglect in 11 (9.5 %; L/R: 2/9), visual agnosia in 10 (8.5 %; L/B: 7/3), prosopagnosia in 7 (6 %; R/B: 4/3), and color dysnomia in 6 (5 %; L: 6). CONCLUSIONS: s-PCAIs are uncommon, representing less than a third of all PCA infarctions. Although embolism is the main cause in 60 % of patients, identification of the emboli source is often not possible. In 1/3 of cases, the stroke mechanism cannot be determined. Neuropsychological deficits are frequent if systematically searched for.
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Cardiovascular autonomic functions were investigated in a prospective, controlled study of 22 consecutive relapsing-remitting multiple sclerosis (MS) patients and 22 healthy subjects using 5 simple noninvasive tests and sympathetic skin response testing. Tests included the heart rate response to deep breathing, valsalva maneuver and standing, blood pressure response to standing and sustained hand grip, and were graded according to the Ewing and Clark classification as early, definite or severe impairment. The relationship between autonomic dysfunction and disease-related parameters such as the expanded disability status scale (EDSS) and disease duration was studied. Ninety percent of the patients had symptoms related with autonomic dysfunction, and 45.5 % had abnormal results in cardiovascular autonomic function testing with 4 patients also having abnormal sympathetic skin responses. Statistical analysis indicated that patients with a long disease duration rather than high EDSS carried a risk of autonomic involvement in MS. Both parasympathetic and sympathetic functions were impaired and this could have been easily overlooked by a standard EDSS follow-up. In this regard, autonomic function testing seems necessary in order to detect subclinical changes in MS patients and should be considered in outcome measures.
Among 4200 consecutive patients admitted to three hospitals with acute ischemic stroke, we found only 11 patients in whom magnetic resonance imaging (MRI) had proved that they had medial medullary infarction (MMI). In our centers, patients with MMI were less than 1% of those with vertebrobasilar stroke. The infarcts documented by MRI were unilateral in 10 patients and bilateral in one. On clinico-topographical analysis there were four clinical patterns: (1) Classical Dejerine's syndrome was the most frequent, consisting of contralateral hemiparesis, lemniscal sensory loss and ipsilateral lingual palsy in 7 of the eleven patients. (2) Pure hemiparesis was present in 2 patients; (3) Sensorimotor stroke was present in 1 patient with contralateral hemiparesis, hypesthesia and mild decrease in pain sensation without lingual palsy; (4) Bilateral MMI syndrome in 1 patient, accompanied by tetraparesis, bilateral loss of deep sensation, dysphagia, dysphonia and anarthria. Presumed causes of MMI were intrinsic branch penetrator artery disease with concomitant vertebral artery stenosis in 6 of the 11 patients, vertebral artery occlusion in 2, dolichoectatic vertebrobasilar arteries in 2, a source of cardiac embolism in 1. Prognosis at 3 months was favorable in 8 patients, but the patient with bilateral MMI syndrome had persisting motor deficit causing limitation of daily activities, and 2 died from systemic causes. The classical triad of acute MMI facilitates the diagnosis, although the recognition of this syndrome in patients with incomplete manifestations can be difficult and occurs more frequently than commonly thought. Moreover, vertebral artery atherosclerosis and branch atheromatous disease of the penetrating arteries are the main causes of medullary infarction.