Cerebral foreign body granulomas after mechanical thrombectomy: Two case reports and a review of the literature.

OBJECTIVES: A foreign body granuloma after an endovascular intervention is a rare complication. Some cases of foreign body granulomas, especially after coil embolization, have been reported. However, only four cases of foreign body granulomas after mechanical thrombectomy (MT) have previously been reported. The current study reports two cases of post-MT foreign body granulomas, including a biopsy-proven case. MATERIAL AND METHODS: Case 1: A 73-year-old woman presented with complete occlusion of the right middle cerebral artery. Cerebral angiography and MT were successfully performed with improvement in clinical symptoms. Left hemiparesis and a disturbance in attention appeared after discharge and progressed slowly. She was re-admitted to our hospital 120 days after cerebral infarction owing to foreign body granulomas diagnosed on biopsy. Case 2: A 78-year-old man presented with occlusion of the left cervical internal carotid artery and the left middle cerebral artery. Cerebral angiography, percutaneous transluminal angioplasty, and MT were successfully performed. On the 34th day, he experienced progressive consciousness disorder because of foreign body granulomas. Both cases were successfully treated with steroid therapy. RESULTS: MRI after steroid treatment showed the disappearance of most nodular lesions and improvement of the encephalopathy. CONCLUSIONS: The cause of the granuloma may be an allergic reaction to the hydrophilic polymers that peel from endovascular devices. Steroid therapy is an effective treatment; therefore, neurologists should consider this complication when neurological symptoms or signs on image appears or worsens. A reliable diagnosis is important for prompt treatment.

Cerebral perfusion changes in chronic dizziness: A single-photon emission computed tomography study.

BACKGROUND AND PURPOSE: Dizziness may persist even after the causative vestibular imbalance subsides. Although the precise mechanism of chronic dizziness is unknown, various cerebral activity changes associated with it have been reported. To understand its mechanism in the absence of the causative vestibular imbalance, we compared cerebral changes in chronic dizziness with and without persistent vestibular imbalance. METHODS: Between September 2014 and March 2020, we examined regional cerebral blood flow (rCBF) in 12 patients having chronic post-lateral medullary infarction dizziness with persistent brainstem vestibular imbalance and 23 patients having chronic dizziness without currently active vestibular imbalance using single-photon emission computed tomography (SPECT) with 99m Technetium-ethyl cysteinate dimer. Further, we analyzed the SPECT images using a voxel-based group comparison. RESULTS: We observed a decreased rCBF in the occipital lobe and increased rCBF in the medial and inferior parts of the temporal lobe in patients having chronic dizziness with and without active vestibular imbalance compared to healthy controls. However, only patients having chronic dizziness without active vestibular imbalance exhibited increased rCBF in the frontal lobe, including the orbitofrontal cortex. CONCLUSION: This is the first study to highlight the difference in rCBF changes between patients having chronic dizziness with and without active vestibular imbalance. Decreased occipital lobe activity and increased medial and inferior temporal lobe activity may be related to keeping dizziness perception triggered regardless of the presence or absence of active vestibular imbalance, whereas increased frontal lobe activity may explain the dizziness background to persist after the disappearance of vestibular imbalance.

[Hypoglycemia].

Hypoglycemia may lead to acute hemiplegia. The most common diffusion-weighted MRI finding in patients with hypoglycemic hemiplegia is a hyperintense internal capsule lesion, which mimics acute ischemic stroke. In addition to the internal capsule lesion, various MRI findings have been reported in patients with hypoglycemia(including hyperintense lesions in the cerebral cortex, basal ganglia, subcortical white matter, and splenium of the corpus callosum). It has recently been reported that hypoglycemic brain damage starts in the large white matter tracts, such as the internal capsule, and spreads to the entire brain, including the gray matter. However, the mechanism underlying the development of focal signs, such as hemiplegia in metabolic disorders, which affects the entire brain, remains unclear.

Influence of Platelet Aggregate Formation in Blood Samples on Light Transmission Aggregometry Results.

BACKGROUND: Light transmission aggregometry is a standard method used to evaluate platelet function. However, in clinical settings, light transmission aggregometry results sometimes fail to reflect actual platelet hyperactivity. In patients with suspected platelet hyperactivity such as thrombosis, platelet aggregates are frequently detected in citrated blood samples using a scattergram of a hematology analyzer. This study aimed to evaluate the effects of platelet aggregate formation on light transmission aggregometry results. METHODS: We used 19 citrated blood samples in which platelet aggregate formation was intentionally induced by a hematology analysis process. Employing fully automated light transmission aggregometry and agonists including adenosine diphosphate or collagen, light transmission aggregometry maximum aggregation percentage, platelet count, and mean platelet volume of platelet-rich plasma before and after platelet aggregate formation were evaluated. RESULTS: Light transmission aggregometry maximum aggregation percentage with adenosine diphosphate or collagen was significantly lower in the samples after than before platelet aggregate formation. Platelet count and mean platelet volume were both decreased by platelet aggregate formation (P < .01), suggesting that maximum aggregation percentage reduction was caused by the decrease in activated large platelets in the platelet-rich plasma. CONCLUSION: This study clarified that platelet aggregate formation in blood samples interfered with an accurate assessment of platelet hyperactivity. To ensure reliability of light transmission aggregometry results, we must confirm that platelet aggregates have not formed in the sample, especially in those of patients with platelet hyperactivity.

Changes in stroke risk by freedom-from-stroke time in simulated populations with atrial fibrillation: Freedom-from-event effect when event itself is a risk factor.

The risk of atrial fibrillation (AF)-related stroke is usually assessed by calculating the CHA2DS2-VASc score, the components of which are various risk factors, including prior stroke. Although prior stroke is considered the strongest risk factor, the associated risk is actually inferred. Nevertheless, it implies a "freedom-from-event effect" (FEE)-the longer a patient is stroke-free, the lower the stroke risk. Although dynamic prognostication has been applied to cancer, the FEE has been ignored in AF, probably because of methodological difficulties. We conducted a simulation study to evaluate the FEE in the risk of AF-related stroke. We modeled various populations of AF patients and simulated the development of stroke assuming a nonhomogeneous Poisson process, where the hazard depends on age, comorbidities, and individual variability. Parameters were set so that the model respects the CHA2DS2-VASc scoring scheme and reproduces the 1-year CHA2DS2-VASc score-wise stroke risk and relative risk conferred by real-world risk factors. We tracked stroke risk over 0 to 15 years of freedom-from-stroke time (FST), both prospective FST (pFST), which begins at the time of diagnosis and continues to the future, and retrospective FST (rFST), which begins at the present and looks backward to the time of diagnosis. The pFST counterbalanced the increase in stroke risk conferred by aging; in patients with a CHA2DS2-VASc score of 1, the pFST offset 62% of the age-conferred risk increase. The rFST reduced the stroke risk; in patients with a CHA2DS2-VASc score of 2 and without prior stroke, an rFST of 6.8 years reduced the stroke risk to the midpoint between CHA2DS2-VASc scores 1 and 2. The study results suggest that the FEE should be considered in evaluating stroke risk in patients with AF. The FEE may be important in other recurrent diseases for which a prior event is a risk factor for a future event.

Common and specific risk factors for ischemic stroke in elderly: Differences based on type of ischemic stroke and aging.

BACKGROUND: The risk factors among the types of ischemic stroke (atherothrombotic cerebral infarction: ATI, cardio-embolic infarction: CEI, lacunar infarction: LI) in aged stroke patients have rarely been compared to each other. METHODS: We compared the clinical parameters of 300 elderly patients with ischemic stroke, age 65-98years, to 100 age-matched control patients. RESULTS: Comparison by parametric test and logistic regression analysis between all 300 and 100 control patients showed higher systolic and diastolic blood pressures (p<0.001, p=0.03), lower estimated glomerular filtration rate (eGFR) (p=0.01), larger cardiothoracic ratio (CTR) (p<0.001), smoking (p<0.01) and possibly poor adherence to anti-hypertensive agents in the ischemic stroke patients (p<0.001). Comparisons among three types (n=100 for each) showed the highest atheromatous risk factors for ATI to be hemoglobin A1c (p=0.01) and low-density lipoprotein (p<0.001) and for CEI to be largest cardiac load, indicated by largest left atrial dimension (p<0.001), and CTR (p<0.001). Triglyceride level was found to be a borderline risk factor for LI (p=0.054). Comparison between those aged <74 versus ≥75years (n=150 for each) showed a lower eGFR (p=0.02) and larger right atrial dimension (p<0.001) in patients ≥75. CONCLUSION: The risk factors were quite different among the subtypes and aging.

Rapidly progressive dementia caused by a superior sagittal sinus dural arteriovenous fistula: a case report.

We describe the case of a 72-year-old man who presented with dementia that had progressed rapidly over a few months. Laboratory analysis of blood and cerebrospinal fluid (CSF) showed no abnormalities, with the exception of a slightly increased CSF protein level. Results of routine magnetic resonance imaging (MRI) including diffusion-weighted imaging (DWI) and magnetic resonance angiography (MRA) were unremarkable. However, detailed neuroimaging studies including contrast-enhanced T1-weighted MRI and conventional angiography revealed a superior sagittal sinus (SSS) dural arteriovenous fistula (DAVF). After endovascular embolization and surgical interruption of all arteries feeding the DAVF, the dementia reversed. We should be aware of the possibility of DAVF as the cause of rapidly progressive dementia even if routine MRI reveals no or only minimal abnormality.

Hemichorea in a thymoma patient without anti-CRMP-5 antibody.

We reported a 72-year-old man with thymoma who presented with hemichorea. Although his brain CT and MRI revealed no abnormality, regional cerebral blood flow changes, identified by single photon emission computed tomography, suggested that the mechanism underlying the chorea seemed to be a dysfunction of the subthalamic nucleus and pallidum. His hemichorea was completely resolved after thymectomy. Absence of serum anti-neural autoantibodies, including small-cell lung carcinoma-related chorea anti-CRMP-5 antibody, suggests that mechanisms different from cross-talk neural-targeted tumor immune response can be responsible for the thymoma-associated paraneoplastic chorea.

Pseudo-subarachnoid hemorrhage in cryptococcal meningitis: MRI findings and pathological study.

A pseudo-subarachnoid hemorrhage (pseudo-SAH) is a brain computed tomography (CT) finding that is seen as high-density areas along the basal cisterns, the sylvian vallecula/fissure, the tentorium cerebella, or the cortical sulci, although no SAH is found upon lumbar puncture or at autopsy. There is one report of cryptococcal meningitis presenting as pseudo-SAH, but the explanatory pathology is unknown. A 68-year-old woman with headache, fever, decreased hearing, and decreased vision was admitted to our hospital. Cerebrospinal fluid India ink staining was positive, and culture yielded Cryptococcus neoformans. Cryptococcus meningitis was diagnosed. Head CT and magnetic resonance imaging (MRI) showed no abnormality upon admission, but 1 month later, head CT showed iso- to high-density areas within the sulci, and fluid-attenuated inversion recovery MRI showed high signal intensity within the convexity sulci resembling an SAH. These areas were enhanced by gadolinium on T1-weighted images. Lumber puncture produced no evidence of bleeding. Biopsy of the left frontal lobe sulci was performed, and histopathological study revealed inflammation and granulation with capsules of C. neoformans. The inflammation and granulation at the convexity sulci induced by the C. neoformans infection explained the pseudo-SAH in this case. Physicians should be aware that cryptococcal meningitis-induced inflammation and granulation at the sulci can present as pseudo-SAH on CT and MRI.

The spectrum of clinicopathological features in pure autonomic neuropathy.

We assessed the clinicopathological features of nine patients with pure autonomic neuropathy, that is, neuropathy without sensory or motor deficits. The duration from symptom onset to diagnosis ranged from 1 month to 13 years. Of eight patients in whom serum antiganglionic acetylcholine receptor antibody was determined, four were positive. All patients who tested positive for this antibody manifested widespread autonomic dysfunction, with the exception of one patient who only experienced orthostatic hypotension. However, patients who were negative for the antiganglionic acetylcholine receptor antibody presented with partial autonomic failure. One of these patients had diffuse parasympathetic failure and generalized hypohidrosis but no orthostatic hypotension, which is clinically compatible with postganglionic cholinergic dysautonomia. Electron microscopic examination revealed a variable degree of reduction in unmyelinated fibers. Compared with normal controls, the patients had a significantly increased density of collagen pockets (p < 0.05). Additionally, the percentage of Schwann cell subunits with axons (out of the total number of Schwann cell subunits associated with unmyelinated fibers) was significantly decreased (p < 0.01). The density of unmyelinated fibers tended to decrease with increasing time between the onset of autonomic symptoms and biopsy (p < 0.05). In conclusion, the clinical and pathological features of pure autonomic neuropathy vary in terms of progression, autonomic involvement, presence of the antiganglionic acetylcholine receptor antibody, and loss of unmyelinated fibers.

Conservative treatment of ruptured vertebrobasilar dissecting aneurysm.

Ruptured vertebrobasilar dissecting aneurysm is usually treated surgically because rebleeding negatively affects outcome. However, the risk of rebleeding decreases markedly once several hours have passed from the initial bleeding. Moreover, surgery-related complications are not rare. We describe seven patients with ruptured vertebrobasilar dissecting aneurysm. To prevent rebleeding during the acute stage, we treated all seven patients conservatively with fentanyl instead of emergency surgery. During the follow-up period (mean 20 months), no patient suffered rebleeding. Conservative treatment with fentanyl administration may be a good option for management of ruptured vertebrobasilar dissecting aneurysm during the acute stage.