Shinri Oda

Asymptomatic versus Symptomatic Infarcts from Vasospasm in Patients with Subarachnoid Hemorrhage: Serial Magnetic Resonance Imaging

OBJECTIVE By use of serial magnetic resonance imaging (MRI), we prospectively investigated the incidence of and the risk factors associated with infarction caused by vasospasm with or without a delayed ischemic neurological deficit (DIND) in patients with subarachnoid hemorrhage (SAH). METHODS In 125 patients who underwent surgery for early aneurysms, postoperative MRI scans were obtained at four time points. We defined an infarct from vasospasm as a new lesion not present on the initial MRI within 3 days after SAH and therefore not attributable to primary brain damage or surgical complications. RESULTS Overall, symptoms of infarction (i.e., DIND) occurred in 38% of patients (48 of 125); DIND with a new infarct on MRI was evident in 34% (43 patients), whereas 4% (5 patients) showed no new lesion but had a DIND. However, 29 patients (23%) showed a new infarct but no DIND on MRI studies (asymptomatic infarction). Asymptomatic ischemic lesions due to vasospasm tended to involve noneloquent brain areas in the territory of intraparenchymal perforators. Multivariate analysis identified variables associated with symptomatic infarction to be of poor SAH grade, advanced age of the patient, angiographic findings of vasospasm, multiple cortical infarcts on MRI studies consistent with vasospasm, and chronic hydrocephalus. CONCLUSION Analysis of the data confirmed the occurrence of asymptomatic infarcts due to vasospasm. These infarcts often developed in noneloquent areas representing perforator territory. MRI investigation of vasospastic lesions referable to intraparenchymal vessels such as perforators complements the study of extraparenchymal major vessel vasospasm in patients with SAH by computed tomographic angiography.

Development of akinetic mutism and hyperphagia after left thalamic and right hypothalamic lesions

A case of childhood post-traumatic akinetic mutism is presented. The patient showed a hyperphagic condition while recovering from akinetic mutism. He had lesions in the left interlaminal nucleus of the thalamus, right globus pallidus, and right dorsomedial nucleus of the hypothalamus. Laboratory data indicated slightly disturbed hypothalamic functions. In general, akinetic mutism can be seen with bilateral destructive lesions, while hyperphagia may occur after destruction of dorsomedial hypothalamic nucleus, but it is very rare. This is the first reported case of akinetic mutism caused by a unilateral lesion.

Early aneurysm surgery and dehydration therapy in patients with severe subarachnoid haemorrhage without ICH.

SummaryWe prospectively analysed treatment results in patients with severe subarachnoid haemorrhage (SAH) who underwent early aneurysm surgery, and were managed by dehydration therapy. We studied a total of 31 patients with poor-grade SAH including 18 in grade IV, and 13 in grade V according to the WFNS classification system. Patients who were older than 70 years of age, or those with an intracerebral haemorrhage or absent brainstem response were excluded from this study. At surgery, clot evacuation from the peribrainstem cisterns with/without external decompression was performed following obliteration of the aneurysmal neck. In the early postoperative period, patients were maintained in negative water balance using osmotic diuretics. When delayed ischaemic deficits had manifested themselves, the pulmonary wedge pressure and/or central venous pressure was immediately increased by the rapid injection of albumin until hypovolaemia reverted to normovolaemia with the continuous administration of dobutamine. The outcome at 3 months was good recovery in 16 (52%) patients, moderate disability in 3 (10%), severe disability in 5 (16%), a vegetative state in 1 (3%), and death in 6 (19%). We thought that early aneurysm surgery and postoperative dehydration therapy in the acute stages of brain oedema resulting from primary brain damage are effective in the treatment of patients with severe SAH but reversilbe primary brain damage.

Early infarction detected by diffusion-weighted imaging in patients with subarachnoid hemorrhage

PurposeEarly infarction that occurs at the time of initial subarachnoid hemorrhage (SAH) due to rupture of an aneurysm is a poorly understood phenomenon. We investigate the frequency of early infarction using diffusion-weighted images (DWI) at the time of admission. We then discuss the pathogenesis of infarction.Materials and methodsThis study included 85 SAH patients who underwent serial DWI on admission. Early infarction detected by DWI and clinical features were investigated retrospectively.ResultsThe overall incidence of DWI-detected early infarction at the time of SAH onset was 8% (7 of 85 cases). In all seven patients, early infarctions were asymptomatic on admission. Types of early infarction seen on DWI included infarcts occurring in the territory of the vessel harboring a ruptured aneurysm (solitary, three cases) and infarcts occurring outside the territory of the vessel (multiple, two cases; solitary, two cases). Six of seven patients eventually developed delayed ischemic neurological deficit (DIND) and computed tomography (CT)-detected and DWI-detected delayed extensive infarction. Four of seven patients with early infarction had an unfavorable outcome. The occurrence of DWI-detected early infarction on admission was significantly correlated with delayed angiographic vasospasm, DIND, CT-detected delayed infarction, DWI-detected delayed infarction, and unfavorable outcome.ConclusionsIn the present study, DWI-detected early infarction at the time of SAH onset was correlated with the occurrence of delayed extensive ischemic lesions. We believe that performing DWI at the time of admission is useful for evaluating the primary ischemic insult, which might play an important role in the pathogenesis of early brain injury and delayed vasospasm-related complications.

Neuroradiologic Diagnosis of Minor Leak prior to Major SAH: Diagnosis by T1-FLAIR Mismatch

BACKGROUND AND PURPOSE: In major SAH, the only method to diagnose a preceding minor leak is to ascertain the presence of a warning headache by interview; however, poor clinical condition and recall bias can cause inaccuracy. We devised a neuroradiologic method to diagnose previous minor leak in patients with SAH and attempted to determine whether warning (sentinel) headaches were associated with minor leaks before major SAH. MATERIALS AND METHODS: We retrospectively evaluated 127 patients who were admitted with SAH within 48 hours of ictus. Previous minor leak before major SAH was defined as T1WI-detected clearly bright hyperintense subarachnoid blood accompanied by SAH blood on FLAIR images that was distributed over a larger area than bright hyperintense subarachnoid blood on T1WI (T1-FLAIR mismatch). RESULTS: The incidence of warning headache before SAH was 11.0% (14 of 127 patients, determined by interview). The incidence of T1-FLAIR mismatch (neuroradiologic diagnosis of minor leak before major SAH) was 33.9% (43 of 127 patients). Of the 14 patients with warning headache, 13 had a minor leak diagnosed by T1-FLAIR mismatch at the time of admission. Variables identified by multivariate analysis as significantly associated with minor leak diagnosed by T1-FLAIR mismatch included 80 years of age or older, rebleeding after admission, intracerebral hemorrhage on CT, and mRS scores of 3–6. CONCLUSIONS: We conclude that warning headaches diagnosed by interview are not a product of recall bias but are the result of actual leaks from aneurysms.

Discrepancy of xenon concentrations between end-tidal and blood collection methods in xenon-enhanced computed tomographic measurement of cerebral blood flow

SummaryUsing xenon-enhanced computed tomography for the study of cerebral blood flow, simultaneous measurements of end-tidal and arterial blood xenon concentrations using the blood collection method were performed to investigate the validity of substituting the end-tidal for the arterial blood xenon concentration. Simultaneous measurement by both methods was performed 68 times in 27 patients. There was no statistical correlation between the arterial blood accumulation rate constant obtained by arterial blood and end-tidal samples, nor between the arterial blood saturation value obtained by the two methods, even when correction was made for age. In brain tissue, all parameters calculated using the end-tidal concentration were lower than those using arterial blood. We therefore suggest that cerebral blood flow values calculated using end-tidal xenon concentration are useful only for qualitative cerebral blood flow mapping, and not applicable to absolute values of cerebral blood flow.

MRimaging findings after ventricular puncture in patients with SAH.

Summary Object. Using magnetic resonance (MR) imaging, we studied brain injury from ventricular puncture performed during craniotomy in the acute stage of subarachnoid hemorrhage (SAH). Methods. 80 patients underwent craniotomy for aneurysm obliteration within 48 hr after SAH, ventricular puncture for drainage of cerebrospinal fluid (CSF) was perfomed to reduce intracranial pressure. MR imaging was performed within 3 days following surgery to measure the size of the lesion, and was repeated on postoperative days 14 and 30. Conclusions. Of the 80 patients with ventricular puncture preceding craniotomy, 65 (81%) showed MR evidence of brain injury from the puncture. Overall, 149 lesions were detected. According to coronal images, cortical injuries (54 cases), penetrating injury to tracts along the ventricular tube (55 cases), caudate injury (25 cases), and corpus callosum injury (15 cases). Brain injuries from ventricular puncture did not correlate significantly to patient outcome. While ventricular puncture and drainage of CSF can readily be performed to decrease brain volume at the time of craniotomy in acute-stage SAH, neurosurgeons should be aware of a surprisingly high incidence of brain injury complicating puncture.

Centripetal Propagation of Vasoconstriction at the Time of Headache Resolution in Patients with Reversible Cerebral Vasoconstriction Syndrome

In this retrospective cohort study, the authors evaluated 16 patients diagnosed with reversible cerebral vasoconstriction syndrome who underwent MR imaging, including MRA, within 72 hours of RCVS onset (initial MRA) and within 48 hours of thunderclap headache remission. In 14 of the 16 patients (87.5%), centripetal propagation of vasoconstriction occurred from the initial MRA to remission of thunderclap headache, with typical segmental vasoconstriction of major vessels (M1, P1, A1). The authors conclude that there is evidence of centripetal propagation of vasoconstriction on MRA performed at the time of remission of the thunderclap headache, and this time point may represent a useful opportunity to diagnose RCVS with greater confidence. BACKGROUND AND PURPOSE: Reversible cerebral vasoconstriction syndrome is characterized by thunderclap headache and diffuse segmental vasoconstriction that resolves spontaneously within 3 months. Previous reports have proposed that vasoconstriction first involves small distal arteries and then progresses toward major vessels at the time of thunderclap headache remission. The purpose of this study was to confirm centripetal propagation of vasoconstriction on MRA at the time of thunderclap headache remission compared with MRA at the time of reversible cerebral vasoconstriction syndrome onset. MATERIALS AND METHODS: Of the 39 patients diagnosed with reversible cerebral vasoconstriction syndrome at our hospital during the study period, participants comprised the 16 patients who underwent MR imaging, including MRA, within 72 hours of reversible cerebral vasoconstriction syndrome onset (initial MRA) and within 48 hours of thunderclap headache remission. RESULTS: In 14 of the 16 patients (87.5%), centripetal propagation of vasoconstriction occurred from the initial MRA to remission of thunderclap headache, with typical segmental vasoconstriction of major vessels. These mainly involved the M1 portion of the MCA (10 cases), P1 portion of the posterior cerebral artery (10 cases), and A1 portion of the anterior cerebral artery (5 cases). CONCLUSIONS: This study found evidence of centripetal propagation of vasoconstriction on MRA obtained at the time of thunderclap headache remission, compared with MRA obtained at the time of reversible cerebral vasoconstriction syndrome onset. If clinicians remain unsure of the diagnosis during early-stage reversible cerebral vasoconstriction syndrome, this time point represents the best opportunity to diagnose reversible cerebral vasoconstriction syndrome with confidence.

Endoscopic Endonasal Approach to the Middle Cranial Fossa through the Cavernous Sinus Triangles: Anatomical Considerations

The lateral limit of endoscopic endonasal surgery has yet to be defined. The aim of this study was to investigate the lateral limit of endoscopic endonasal surgery at the level of the sphenoid sinus. Access from the sphenoid sinus to the middle cranial fossa through the cavernous sinus triangles was evaluated by cadaver dissection. Anatomical analysis demonstrated that the medial temporal dura mater was exposed through the anterior area of the clinoidal triangle, anteromedial triangle, and superior area of the anterolateral triangle, indicating potential corridors to the middle cranial fossa. This study suggests that the cavernous sinus triangles are applicable in selected cases to manage middle cranial fossa lesions by endoscopic endonasal surgery.

Identification of the internal carotid artery at the superior part of the cavernous sinus during endoscopic endonasal cavernous sinus tumor surgery

BackgroundIdentification of the internal carotid artery (ICA) is essential for successful endoscopic endonasal cavernous sinus tumor surgery. This study aimed to develop a method for identifying the ICA in cavernous sinus tumors at the superior part of the cavernous sinus.MethodsTen fresh cadavers were studied with a 4-mm 0° and 30° endoscope to identify surgical landmarks of the ICA in the cavernous sinus. Clinical cases of cavernous sinus tumors were surgically treated using an endoscopic transpterygoid approach.ResultsAnatomical study indicated the ICA at the superior part of the cavernous sinus can be identified using three steps: 1) exposure of the optic nerve sheath by drilling the optic canal; 2) identification of the proximal orifice of the optic nerve sheath at the transition of the optic nerve sheath and dura mater of the tuberculum sellae; and 3) identification of the clinoid segment of the ICA at the distal dural ring just below the proximal orifice of the optic nerve sheath. Although the ICA was encased and transposed by tumors in preliminary surgical cases, the clinoid segment of the ICA was safely exposed at the superior part of the cavernous sinus using this method.ConclusionsDural structures around the cavernous sinus are key to identifying the ICA at the superior part of the cavernous sinus. This method is expected to reduce the risk of ICA injury during endoscopic endonasal surgery for cavernous sinus tumors.