1/9. Transient aphasia and persistent amnesia after surgery for internal carotid artery--posterior communicating artery aneurysm.We report a case of transient aphasia and persistent amnesia after clipping of a ruptured cerebral aneurysm to treat a subarachnoid hemorrhage. Postoperatively, aphasia was identified and magnetic resonance imaging (MRI) showed an abnormal intensity area in the left anterior thalamus. Single photon emission computed tomography (SPECT) revealed a wider area of low perfusion surrounding the left thalamus and left frontotemporal lobe than that shown by the MRI. His aphasia resolved over the subsequent 12-week period. He was left with an isolated disturbance of memory; in the absence of any dementia, aphasia or disturbance of consciousness, his condition was classified as one of amnesia. SPECT 14 weeks after admission revealed an area of low perfusion limited to the left thalamus. These findings suggest that the persistence of amnesia in this case was caused by the infarction of the mammillothalamic tract, and the recovery from aphasia may have resulted from the disappearance of surrounding edema.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
2/9. Neuropsychological manifestations in a case of bilateral thalamic infarction.Neuropsychological manifestation has been reported with lesions of the anterior and non-specific thalamic nuclei and mammilothalamic tract (MMT). These have been reported in the setting of arterial infarction and/or haemorrhage. Cerebral venous sinus thrombosis (CVT) is a rare cause of brain infarction. It occurs in the setting of oral contraceptive administration or pregnancy. Inherited thrombophilias are documented risk factors. The most frequent being heterozygous factor v Leiden mutation. We report a single case of bilateral thalamic infarction due to cerebral vein and sinus thrombosis. Clinically the case manifested with memory impairment and dysexecutive symptoms. Predisposing factor for venous thrombosis was a homozygous factor v Leiden mutation. The patient was treated with anticoagulation and made a good recovery.- - - - - - - - - - ranking = 0.30189168026637keywords = haemorrhage (Clic here for more details about this article) |
3/9. Deterioration of pre-existing hemiparesis brought about by subsequent ipsilateral lacunar infarction.Mechanisms of post-stroke recovery are still poorly understood. Recent evidence suggests that cortical reorganisation in the unaffected hemisphere plays an important role. A 59 year old man developed a small lacunar infarct in the left corona radiata, which then caused marked deterioration in a pre-existing left hemiparesis that had resulted from an earlier right putaminal haemorrhage. Functional magnetic resonance imaging showed that the paretic left hand grip activated the ipsilateral left motor areas, but not the right hemispheric motor areas. This suggests that partial recovery of the left hemiparesis had been brought about by cortical reorganisation of the left hemisphere and intensification of the uncrossed corticospinal tract. The subsequent small infarct may have damaged the uncrossed tract, thereby causing the pre-existing hemiparesis to deteriorate even further.- - - - - - - - - - ranking = 0.30189168026637keywords = haemorrhage (Clic here for more details about this article) |
4/9. Central deafness associated with a midbrain lesion.Central deafness has been linked historically to bihemispheric involvement of the temporal lobe, with more recent findings suggesting that compromise of other cortical and subcortical structures can also result in this disorder. The present investigation extends our understanding of the potential anatomical correlates to central deafness by demonstrating that bilateral involvement of an auditory structure within the midbrain can additionally result in this condition. Our subject was a 21-year-old male with a subarachnoid bleed affecting both inferior colliculi. Significant auditory deficits were noted for the middle and late auditory evoked potentials, while electrophysiologic measures of the periphery indicated normal function. The patient was enrolled in a rehabilitation program for approximately 14 weeks. Although initially unresponsive to sounds, the patient regained most of his auditory abilities during the 10 months he was followed. This case documents the range of auditory deficits that may be associated with damage to the inferior colliculi, and it profiles a hierarchical recovery of auditory function consistent with test findings.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
5/9. CNS aspergillosis with mycotic aneurysm, cerebral granuloma and infarction.We are reporting a case of an immunocompromised patient with invasive aspergillosis (IA) who developed aspergillotic granulomas and a mycotic aneurysm of the superior cerebellar artery. The route of infection of the central nervous system (CNS) was hematogenous spread from a pulmonary focus. IA was detected with the Galactomannan (GM) technique. However, despite treatment with amphotericin b, progressive involvement of the vessel wall occurred causing fatal subarachnoid hemorrhage and massive brainstem and cerebellar infarction.This case provides pathologic-imaging correlation of one of the most devastating types of fungal involvement affecting the CNS with a fungal aneurysm. Finally the literature regarding the pathogenetic, and diagnostic investigations and the management of CNS aspergillosis is reviewed.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
6/9. Thrombosed unruptured cerebral aneurysm causing brain infarction followed by subarachnoid hemorrhage--case report--.A 71-year-old man presented with right hemiparesis and aphasia due to cerebral infarction in the frontal lobe. Computed tomography (CT) revealed a high-density mass, 12 mm in diameter, in the stem of the left sylvian fissure. Carotid angiography demonstrated occlusion of the left ascending frontal artery complex and retention of contrast medium at the bifurcation of the left middle cerebral artery (MCA). The diagnosis was cerebral infarction caused by occlusion of the ascending frontal artery complex resulting from thrombosed left MCA aneurysm. The patient was managed conservatively and his neurological symptoms gradually improved. One month later, he lapsed into a coma. CT revealed subarachnoid hemorrhage. Carotid angiography showed a large left MCA aneurysm with branch occlusion of the left ascending frontal artery complex. A left frontotemporal craniotomy was performed. The MCA aneurysm was opened and the intramural thrombi removed, and finally neck clipping was performed. The patient made a good postoperative recovery.- - - - - - - - - - ranking = 5keywords = subarachnoid (Clic here for more details about this article) |
7/9. Thunderclap stroke: embolic cerebellar infarcts presenting as thunderclap headache.Thunderclap headache is known to be a presenting feature of subarachnoid hemorrhage, unruptured intracranial aneurysm, cerebral venous thrombosis, cervical artery dissection, spontaneous intracranial hypotension, pituitary apoplexy, retroclival hematoma, and hypertensive reversible posterior leukoencephalopathy. We describe a case of thunderclap headache in the absence of focal, long-tract, or lateralizing neurological findings, as the primary clinical feature of embolic cerebellar infarcts. This case expands the differential diagnosis of thunderclap headache and reinforces the need for magnetic resonance imaging in the evaluation of such patients, even when neurologic examination, brain computed tomography, and cerebrospinal fluid analysis are normal.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
8/9. Cluster breathing associated with bihemispheric infarction and sparing of the brainstem.OBJECTIVE: To report cluster breathing pattern associated with a nonbrainstem lesion. DESIGN: Case report. SETTING: Neurointensive care unit, St Mary's Hospital, Rochester, Minn. PATIENT: A patient with subarachnoid hemorrhage developed severe, diffuse, distal bilateral middle cerebral artery vasospasm with resultant cortical laminar necrosis and transient cluster breathing.Intervention magnetic resonance imaging revealed bihemispheric lesions but no brainstem lesion. CONCLUSION: Cluster breathing may occur with nonbrainstem lesions.- - - - - - - - - - ranking = 1keywords = subarachnoid (Clic here for more details about this article) |
9/9. Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations.Progressive ischaemic damage in animals is associated with spreading mass depolarizations of neurons and astrocytes, detected as spreading negative slow voltage variations. Speculation on whether spreading depolarizations occur in human ischaemic stroke has continued for the past 60 years. Therefore, we performed a prospective multicentre study assessing incidence and timing of spreading depolarizations and delayed ischaemic neurological deficit (DIND) in patients with major subarachnoid haemorrhage (SAH) requiring aneurysm surgery. Spreading depolarizations were recorded by electrocorticography with a subdural electrode strip placed on cerebral cortex for up to 10 days. A total of 2110 h recording time was analysed. The clinical state was monitored every 6 h. Delayed infarcts after SAH were verified by serial CT scans and/or MRI. Electrocorticography revealed 298 spreading depolarizations in 13 of the 18 patients (72%). A clinical DIND was observed in seven patients 7.8 days (7.3, 8.2) after SAH. DIND was time-locked to a sequence of recurrent spreading depolarizations in every single case (positive and negative predictive values: 86 and 100%, respectively). In four patients delayed infarcts developed in the recording area. As in the ischaemic penumbra of animals, delayed infarction was preceded by progressive prolongation of the electrocorticographic depression periods associated with spreading depolarizations to >60 min in each case. This study demonstrates that spreading depolarizations have a high incidence in major SAH and occur in ischaemic stroke. Repeated spreading depolarizations with prolonged depression periods are an early indicator of delayed ischaemic brain damage after SAH. In view of experimental evidence and the present clinical results, we suggest that spreading depolarizations with prolonged depressions are a promising target for treatment development in SAH and ischaemic stroke.- - - - - - - - - - ranking = 25.783192413735keywords = subarachnoid haemorrhage, subarachnoid, haemorrhage (Clic here for more details about this article) |