Search

This databank-based, multicenter study compared all stroke patients with IV tissue plasminogen activator aged ≥80 years (n = 38) and those

Objective: To describe the clinical and neuroradiologic features and chromosomal mapping of a novel autosomal dominant disease affecting the basal ganglia. Methods: The authors characterized a large family with autosomal dominant basal ganglia disease (ADSD) clinically and by MRI, MR spectroscopy (MRS), and SPECT. The authors performed a whole genome genetic linkage scan to map the underlying genetic defect. Results: The main clinical features of the disease are dysarthria and gait disturbance without any apparent reduction in life expectancy. MRI demonstrated a distinctive lesion pattern restricted mainly to the putamen and caudate nucleus. Genetic linkage analysis localized the causative genetic defect to a 3.25 megabase candidate region on chromosome 5q13.3-q14.1. Conclusions: ADSD is an autosomal dominant basal ganglia disease mapping to chromosome 5q13.3-q14.1.

Few data exist on long-term outcome of patients with cervical aneurysm due to spontaneous dissection of the internal carotid artery (sICAD).1,2 In this prospective observational study, we assessed the long-term risk of stroke, rupture, and development of local symptoms or signs on the side of dissection (headache, neck pain, Horner syndrome, cranial nerve palsy) in cervical aneurysms caused by sICAD. We included 279 consecutive patients with sICAD (diagnosed as previously reported)3 who underwent cerebral MR angiography (MRA; n = 195), digital subtraction angiography (DSA, n = 72), or both (n = 12) at two academic centers from January 1987 until March 2005. Five of these patients died from stroke within 2 weeks after symptom onset; an ICA aneurysm was diagnosed in one of them. A second angiogram (MRA, n = 218; DSA, n = 17; CT angiography, n = 6) was done in 236 (86%) of 274 survivors. Two neurologists blinded to the patients' identity reviewed the angiographies and characterized the aneurysms (localization: postbifurcation, midcervical, or subpetrous third …

We analyzed sex differences in 696 patients with spontaneous cervical artery dissection. There were more men (n = 399; p < 0.0001), and men showed a higher frequency of hypertension (31% vs 15%; p < 0.0001). Women were younger (42.5 +/- 9.9 vs 47.5 +/- 9.3 years; p < 0.0001), had more often multiple dissections (18 vs 10%; p = 0.001), migraine (47 vs 20%; p < 0.0001), and tinnitus (16 vs 8%; p = 0.001). Outcome and mortality were similar in both sexes.

The authors reviewed the histories of 33 patients (ages 44 to 50 years) treated with IV thrombolysis for acute stroke due to spontaneous cervical carotid artery dissection. Median NIH Stroke Scale (NIHSS) score on admission was 15. No new or worsened local signs, subarachnoid hemorrhage, pseudoaneurysm formation, or rupture of the cervical ICA were observed. At 3 months, median NIHSS was 7 and median modified Rankin Scale (mRS) 2.5; mRSor = 2 was observed in 17 patients.

The feasibility and safety of induced arterial hypertension (10 to 20% of the initial value) in the acute phase of ischemic stroke were retrospectively evaluated in 34 patients treated with norepinephrine (NE) for a median of 26 hours. Maximal variability of systolic blood pressure during NE application was within 15% of the target values. Cardiac arrhythmia occurred in one patient, and intracerebral hemorrhage occurred in two patients (fatal in one and asymptomatic in the other). The authors conclude that induced arterial hypertension is feasible and safe in patients with acute stroke.

OBJECTIVE: To compare the rate of ischemic events and intracranial hemorrhage in the long-term follow-up of patients with persistent and transient severe stenosis or occlusion of the internal carotid artery (ICA) due to spontaneous dissection (ICAD). METHODS: One hundred and sixty-one consecutive patients with unilateral ICAD causing severe stenosis or occlusion were examined clinically and by ultrasound 1 year after symptom onset. Forty-six cases with persistent and 46 age- and latency-matched cases with transient (recanalization complete or less than 50% stenosis) severe stenosis or occlusion of the ICA were enrolled. Nine patients with surgical, endovascular, or fibrinolytic therapy for ICAD or associated stroke were excluded. Antithrombotic therapy was given at the discretion of the treating physician. Clinical follow-ups were done annually. RESULTS: Antithrombotic therapy and follow-up were similar in patients with permanent (6.2 +/- 3.4 years) and transient (7.2 +/- 4.3 years) severe stenosis or occlusion of the ICA. Cases with permanent carotid stenosis or occlusion showed annual rates of 0.7% for ipsilateral carotid territory stroke and of 1.4% for any stroke. Cases with transient carotid stenosis or occlusion showed annual rates of 0.3% for ipsilateral carotid territory stroke and of 0.6% for any stroke. CONCLUSIONS: This study suggests that ICAD has a benign long-term prognosis with low rates of ipsilateral carotid territory and any stroke and that the stroke rate in ICAD is not related to the persistence of severe carotid stenosis or occlusion. These results question the rationale of surgical or catheter-based revascularization in patients with ICAD. (Less)

A 48-year-old patient who had aphasia due to a left subcortical hemorrhage underwent three follow-up examinations to assess MR signal changes accompanying recovery. A word classification task was applied. During the 6-month follow-up period, we observed a dynamic change from negative toward positive blood oxygenation level-dependent MR signals, i.e., task-related reafferentation of eloquent cortices occurred. Clinical improvement from aphasia paralleled the MR signal changes.

Objective: To report the safety of acute stent placement in patients with acute ischemic stroke. Background Patients with large vessel occlusions often fail to recanalize with intravenous rt-PA or standard endovascular techniques. Small series have reported excellent recanalization rates with acute stenting. However, its safety is not well known. Design/Methods: We retrospectively reviewed charts of twenty-four consecutive patients treated with stents for large artery occlusions. All eligible patients received intravenous rt-PA before proceeding to endovascular treatment. If there was contraindication to its usage or no neurological improvement occurred after its infusion, the patient underwent immediate angiographic evaluation and treatment. Outcomes were based upon disposition and in-hospital mortality. Results: Twenty-four patients had twenty-seven stents deployed in three scenarios: 1. initial therapy (n=3), 2. after the usage of intra-arterial rt-PA and/or angioplasty (n=19) or 3. as a salvage therapy (n=4). Fourteen patients (58%) received IV rt-PA. The arterial occlusion sites included 11 (44%) proximal M1 middle cerebral artery, 10 (40%) internal carotid artery (8 intracranial, 2 extracranial and 3 involving both), 3 (16%) basilar artery and 1 (4%) vertebral artery. Stents were successfully deployed in 24 out of 27 cases (89%) Poor discharge outcomes were defined as death (n=7), hospice (n=2) or skilled nursing facility (n=5) and occurred in 58% of patients. Good outcomes included home discharge (n=1), inpatient rehabilitation (n=7) or long term acute care facility (n=2) for a total of 42%. The causes attributed to poor outcomes were secondary to either symptomatic intracerebral hemorrhage (sICH) or stroke progression. Five (21%) patients had sICH where any ICH was seen in 14 (58%) total patients. Conclusions: Our results indicate that the usage of acute stentings in ischemic stroke is associated with a high rate of sICH and its routine use is not recommended. Prospective studies regarding the utility and benefits of stents are warranted. Disclosure: Dr. Fong has nothing to disclose. Dr. Bershad has nothing to disclose. Dr. Morsi has nothing to disclose. Dr. Shaltoni has nothing to disclose. Dr. Mawad has nothing to disclose. Dr. Georgiadis has nothing to disclose. Dr. Suarez has received personal compensation for activities with Bristol-Myers Squibb/Sanofi and Boehringer Ingelheim as a speaker. Dr. Suarez has received research support from the Haas Trust and NINDS. Dr. Venkatasubba Rao has nothing to disclose.