1/6. Intracranial clot dissolution is associated with embolic signals on transcranial Doppler. reperfusion of intracranial arteries can be detected by transcranial Doppler (TCD). The authors report microembolic signals (MES) on TCD as a sign of clot dissolution and recanalization. Microembolic signals were detected during routine diagnostic TCD examination performed in the emergency room in patients eligible for thrombolytic therapy. Microembolic signals were found at the site of M1 middle cerebral artery (MCA) high-grade stenosis or near-occlusion. Transcranial Doppler was performed before, during, and after thrombolytic therapy. Of 16 consecutive patients, 3 (19%) had MES on TCD. All three patients had a severe MCA syndrome at 2 hours after stroke onset scored using the National Institutes of health stroke Scale (NIHSS). In patient #1 (NIHSS 12), clusters of MES were detected distal to a high-grade M1 MCA stenosis preceding spontaneous clinical recovery by 2 minutes. Because of subsequent fluctuating clinical deficit, intraarterial thrombolysis was given with complete recovery. In patient #2 (NIHSS 20), TCD detected an M1 MCA near-occlusion. At 1.5 hours after intravenous tissue plasminogen activator, TCD showed minimal MCA flow signals followed by MES, increased velocities, and normal flow signals in just 2 minutes. She gradually recovered up to NIHSS 8 in 5 days. In patient #3 with NIHSS 22 and an M1 MCA near-occlusion, TCD detected MES 15 minutes after TPA bolus followed by MCA flow velocity improvement from 15 cm/sec to 30 cm/sec. The patient recovered completely by the end of tissue plasminogen activator infusion. The authors conclude that embolic signals detected by TCD at the site of arterial obstruction can indicate clot dissolution. Intracranial recanalization on TCD can be associated with MES and changes in flow waveform, pulsatility, and velocity if insonation is performed at the site of arterial obstruction. ( info) |
2/6. Sudden deafness and anterior inferior cerebellar artery infarction. BACKGROUND AND PURPOSE: Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery (AICA) is known to be associated with vertigo, nystagmus, facial weakness, and gait ataxia. Few reports have carefully examined the deafness associated with the AICA infarction. Furthermore, previous neurological reports have not emphasized the inner ear as a localization of sudden deafness. The aim of this study was to investigate the incidence of deafness associated with the AICA infarction and the sites predominantly involved in deafness. methods: Over 2 years, we prospectively identified 12 consecutive patients with unilateral AICA infarction diagnosed by brain MRI. Pure-tone audiogram, speech discrimination testing, stapedial reflex testing, and auditory brainstem response were performed to localize the site of lesion in the auditory pathways. electronystagmography was also performed to evaluate the function of the vestibular system. RESULTS: The most common affected site on brain MRI was the middle cerebellar peduncle (n=11). Four patients had vertigo and/or acute auditory symptoms such as hearing loss or tinnitus as an isolated manifestation from 1 day to 2 months before infarction. Audiological testings confirmed sensorineural hearing loss in 11 patients (92%), predominantly cochlear in 6 patients, retrocochlear in 1 patient, and combined on the affected side cochlear and retrocochlear in 4 patients. electronystagmography demonstrated no response to caloric stimulation in 10 patients (83%). CONCLUSIONS: In our series, sudden deafness was an important sign for the diagnosis of AICA infarction. Audiological examinations suggest that sudden deafness in AICA infarction is usually due to dysfunction of the cochlea resulting from ischemia to the inner ear. ( info) |
3/6. Neurological involvement as a poor prognostic factor in catastrophic antiphospholipid syndrome: autopsy findings in 12 cases. CAPS is an uncommon disease, characterized by clinical evidence of multiple organ involvement and histopathological evidence of multiple vessel occlusions, in patients with either primary or secondary antiphospholipid syndrome. The present series describes the clinical manifestations and autopsy findings of 12 patients with CAPS. Neurological involvement was considered the main cause of death in all of them. CNS pathology revealed thrombotic microangiopathy as well as small and large vessel occlusions in several brain areas. Neurological involvement in CAPS is strongly associated with thrombotic microangiopathy and should be considered a potential cause of death in these patients. ( info) |
| A 37 year-old man who developed a fatal middle cerebral territory infarct was found at autopsy, to have widespread granulomatous angiitis involving meningeal and intracranial--extracerebral vessels but not intracerebral vessels or other extra-cranial vessels. The findings are unique and overlap with those of granulomatous angiitis of the nervous system (GANS) and classic giant cell arteritis (GCA). A possible precipitant for this devastating illness was a recent chlamydia infection. The salient clinical and pathologic differences between GANS and GCA of the nervous system are discussed. ( info) |
5/6. Pulmonary arterial and intracranial calcification in the recipient of a twin-twin transfusion. Pulmonary arterial and intracranial calcifications are rarely found in children. A female infant, the recipient of a twin-twin transfusion syndrome was found, by ultrasound and computed tomography, to have both pulmonary arterial and intracerebral calcification. A rare condition, termed idiopathic arterial calcification of infancy, is the likely cause. This condition carries a poor prognosis and is usually fatal. ( info) |
6/6. Hemorrhagic complications after endovascular therapy for atherosclerotic intracranial arterial stenoses. OBJECTIVE: Hemorrhagic complications were analyzed in 106 procedures of 99 patients treated with percutaneous transluminal angioplasty (PTA) or stenting for intracranial arterial stenoses. methods: Ninety-nine patients with intracranial arterial stenosis were treated with PTA or stenting 106 times from January 1995 to December 2003. Fifty-seven patients had intracranial internal carotid artery stenosis, 23 had middle cerebral artery stenosis, and 19 had vertebrobasilar stenosis. Evaluation of hemodynamic compromise via single-photon emission computed tomography was performed 50 times for 50 patients before the treatment. RESULTS: Four hemorrhagic complications occurred in 106 procedures. Two of these cases involved intracerebral hemorrhage after PTA or stenting in the treated vascular territory 30 minutes and 16 hours after the treatment, respectively. One case showed subarachnoid hemorrhage, which appeared 6 hours after treatment. Hemodynamic compromise was found on single-photon emission computed tomography in these three cases. The last case with a hemorrhagic complication was a hemorrhagic infarction after recanalization of stent thrombosis, which appeared 3 days after stenting. Hyperperfusion syndrome was strongly suggested as the cause of hemorrhage in the two cases associated with intracerebral hemorrhage. CONCLUSION: The rate of hemorrhagic complication directly related to the procedure of PTA or stenting was 3%, and hyperperfusion syndrome was suggested as the cause of hemorrhage in two cases (2%), from the perspective of clinical characteristics and single-photon emission computed tomographic findings. ( info) |