From 2014 to 2015, the five pivotal stroke trials (MR CLEAN, ESCAPE, EXTEND-IA, SWIFT PRIME and REVASCAT) have shown that stroke thrombectomy clearly improved functional outcome of patients with occlusion of the internal carotid artery or the M1 portion of the middle cerebral artery, with a baseline National Institutes of Health Stroke Scale score of ≥6, with a baseline Alberta Stroke Program Early Computed Tomography Score of ≥6, and who could receive thrombectomy within a 6-hour window of symptom onset. In 2018, the efficacy of stroke thrombectomy for patients with late-presenting stroke up to 16 to 24 hours of onset and who had clinical imaging mismatch or target mismatch was also established by the DAWN and the DEFUSE3 trials. Nowadays, stroke thrombectomy, therefore, have become a “standard of care” and acute stroke patients with large vessel occlusion should receive stroke thrombectomy if they meet top-tier evidence criteria.

A significant number of patients with minor or mild stroke symptoms on initial presentation subsequently develop neurological deterioration and poor clinical outcomes at hospital discharge. The presence of an underlying large vessel occlusion is a strong predictor of both clinical worsening and poor outcome. Although patients with a low baseline National Institutes of Health Stroke Scale (NIHSS) could have been included in some randomized controlled trials, the benefits of the mechanical thrombectomy for patients with a low NIHSS score are unknown. The causes of neurological deterioration in patients with underlying large vessel occlusion are heterogeneous, but include collateral failure, and no straightforward mechanisms are found in the majority of cases. Patients with internal carotid artery occlusion, but with a patent middle cerebral artery (MCA), can occasionally have good collateral circulation and develop only minor or mild stroke. These patients exhibit collateral MCA flow via the circle of Willis despite ipsilateral internal carotid artery occlusion. However, thrombus migration may cause occlusion of collateral MCA flow, leading to dramatic neurological deterioration. Careful observation and detailed assessment are required for the management of these patients. Recent studies have examined the efficacy and optimal timing of thrombolysis or mechanical thrombectomy for patients with minor or mild stroke. Herein, we review the mechanisms of neurological deterioration, and the efficacy of reperfusion therapy, for patients with minor or mild stroke.

We herein report a 67-year-old female who presented with progressive dementia and disturbance of consciousness. Brain CT showed multiple subcortical calcifications with edema. Enhanced CT showed multiple abnormal vessels in the left hemisphere. Electroencephalography indicated diffuse spike and slow wave complex, so non-convulsive status epilepticus was diagnosed. Cerebral angiography revealed several feeder arteries with retrograde leptomeningeal venous drainage. We diagnosed her with Borden type III cerebral dural arteriovenous fistulas. Trans-arterial embolization with n-butyl-2-cyanoacrylate was performed, and she has experienced no epileptic attacks for at least ten months. Calcification changes are sometimes seen in Borden type II dural arteriovenous fistulas but not in aggressive types, such as Borden type III. It is important to suspect dural arteriovenous fistulas when we encounter patients with progressive dementia or/and epilepsy with cerebral calcification lesions, as this may be a treatable disease condition.

A 48-year-old woman with a 3-month history of spontaneously resolving stiff leg symptom at the age of 43 years presented with progressive onset of leg rigidity, walking difficulty, and myoclonic jerks. On admission she had marked stiffness in her foot joints with symmetric sustained dorsiflexion of the ankles and toes, with spontaneous and reflex myoclonic jerks easily provoked by knee tendon tap. She appeared to have a spastic gait due to stiffness in her legs. Needle electromyogram (EMG) examination revealed continuous motor unit activity in the tibialis anterior muscle at rest even when voluntary contraction of the gastrocnemius muscle was instructed, but no myokimic discharge or acute denervation sign was seen. The laboratory tests were unremarkable, including glutamic acid decarboxylase antibody. Cerebrospinal fluid (CSF) examination was also normal, without oligoclonal bands or elevated IgG index. She was diagnosed with stiff-limb syndrome based on neurologic examination and needle EMG findings, and she was treated with intravenous high-dose methylprednisolone (500 mg/day, 3 days), resulting in marked improvement in her symptoms. Anti-glycine receptor antibodies were subsequently identified in her archived serum and CSF obtained before immunotherapy. She was then started on oral prednisolone (30 mg/day) and had been free of symptoms.

We report a 77-year-old woman suffering from dementia with Lewy bodies (DLB) who presented with Hashimoto encephalopathy. The patient began to mistakenly believe that another person was sleeping in her bed from approximately 70 years of age. She began to show symptoms of parkinsonism after 75 years of age. One night, the patient began to exhibit loitering behavior, and made incomprehensible comments while also exhibiting other abnormal behaviors. Clinical examination revealed rigidity and tremor of the limbs, as well as hallucination, abnormal speech and behavior. We first considered DLB. However, serum anti-thyroglobulin levels turned out to be elevated, indicating Hashimoto encephalopathy as well, and treated the patient with steroid pulse therapy. Her mental symptoms subsequently improved, but rigidity and tremor remained. ¹²³I-ioflupane SPECT demonstrated decreased accumulation in the bilateral caudal basal ganglia. Anti NH₂-terminal of α-enolase (NAE) antibody in the serum was positive. Therefore, we diagnosed the patient with the rare comorbidity of DLB and Hashimoto encephalopathy, successfully treated with immunotherapy.

A 61-year-old man with squamous cell lung cancer was admitted to our hospital because of consciousness disturbance after treated with pembrolizumab. Cerebrospinal fluid examination revealed increased protein level (209.2 mg/dl) and lymphocytic pleocytosis(79/μl). He was diagnosed as a meningoencephalitis probably caused by an immune-related adverse event (irAE) of immune checkpoint inhibitors (ICIs), and was successfully treated with 1,000 mg methylprednisolone intravenously for 3 days twice and the consequent oral 1 mg/kg prednisolone. As ICIs, which activate the immune systems, are becoming important choices of the treatments against malignancies, we should keep the possibility of irAE in mind and, when needed, start the treatment as soon as possible.

This article was retracted by author’s request.