Previous randomized clinical trials have revealed significant benefit of the endovascular thrombectomy for the patients with acute ischemic stroke. In this short communication, I would like to introduce the history of endovascular treatment for acute ischemic stroke in Japan, and give a positive message to the neurologists who might contribute to the treatment for acute ischemic stroke.
Levodopa-carbidopa intestinal gel (LCIG) therapy has been established as a device-aided treatment for advanced Parkinson’s disease. We retrospectively investigated the issues related to LCIG therapy in patients with Parkinson’s disease at our hospital from March 2014 to July 2018. The subjects were 18 patients including nine men and nine women. The mean duration of PD symptoms and motor fluctuation was 14.5 ± 5.9 and 7.2 ± 4.5 years, respectively. The mean age at initiation of LCIG was 60.1 ± 9.4 years and the mean treatment period was 21.1 ± 19.5 months. One hundred and sixteen LCIG-associated issues were observed, including pain at the gastrostomy site (23 cases), hypergranulation tissue (14 cases), skin redness and/or erosions (11 cases), cutaneous infections at the gastrostomy site (eight cases), percutaneous endoscopic gastrojejunostomy (PEG-J) tube occlusion in the gastrointestinal tract (19 cases), irremovable PEG-J tube (13 cases), dislocation of the PEG-J tube (six cases), and breakage of the connector (eight cases). The majority of these issues were easily diagnosed and could be managed by neurologists who are familiar with LCIG therapy.
Endogenous endophthalmitis is a rare complication of acute meningitis. A healthy 82-year-old woman suddenly developed septic bacteremia and meningitis owing to Staphylococcus aureus (methicillin-susceptible Staphylococcus aureus); she presented with a high fever and drowsiness. Improvement of these initial symptoms unveiled impaired bilateral visual acuity. Detailed ophthalmological assessments diagnosed it as probable endogenous endophthalmitis, which was immediately treated with vitrectomy. Subsequently, the patient totally recovered without any neurologic or ophthalmic sequela.
The case was a 29-year-old male with no previous history of serious disease. He developed headache and fever, which then worsened and he was admitted to our hospital. His temperature was 38.3°C and he had a stiff neck. In cerebrospinal fluid (CSF) tests, the opening pressure was high, the cell count was increased, and the CSF/serum glucose ratio was decreased. In addition, he was positive for cryptococcal antigen. According to these findings, he was diagnosed with cryptococcal meningoencephalitis and antifungal treatment was initiated. His symptoms then improved, but on day 18 after admission, he developed convulsions, and on day 28, right visual field defects appeared. Brain MRI showed disseminated lesions in the bilateral cerebral cortex. Despite a decrease of the cryptococcal antigenic value in the CSF, the IgG index was elevated. IL-6, 8 and 10 in CSF were high levels on Day 1, then gradually reduced as the symptoms improved. But on Day 28, worsening of symptoms, IL-10 was significantly increased dispite IL-6 and 8 reducing. Therefore, the exacerbation of his symptoms and expansion of the lesions were not caused by the Cryptococcus itself, and it was considered that they were due to the late deterioration of cryptococcosis, which responded to steroid treatment.
A 73-year-old women visited emergency department because of sudden right hemiplegia. She had a history of duodenum papilla cancer terminal stage and multiple liver metastasis. On admission, diffusion weighted images revealed high intensity area at left middle cerebral artery territory. In addition, 3D-TOF MRA depicted proximal part of the left internal carotid artery. We performed endovascular thrombectomy because low platelet count met contraindication of intravenous recombinant tissue plasminogen activator therapy. Although we could get partial recanalization of middle cerebral artery occlusion after thrombectomy, the patient eventually died due to multiple organ failure. Autopsy findings showed white thrombus on mitral valve and also left middle cerebral artery occluded by similar white thrombus without infective findings. The patient was finally diagnosed with nonbacterial thrombotic endocarditis due to white thrombus on the mitral valve. We should select appropriate mechanical thrombectomy devices with a case of cerebral infarction due to nonbacterial thrombotic endocarditis because its thrombus is often white thrombus and would be hard.
A 73-year-old man was hospitalized with complaints of general malaise, limb muscle weakness and weight loss progressing in 6 months. Ca, ACE, lysozyme, sIL-2R, vitamin 1.25 D was high in the blood test. Bilateral hilar lymphadenopathy on CT were not recognized, and CD4/CD8 ratio increased by bronchoalveolar lavage. In the 67Ga-citrate scintigraphy, accumulation was observed on the thigh and shoulder to the upper arm bilaterally. A muscle biopsy was performed from the right femoris muscle where the gadolinium contrast effect in the T1 weighted image was observed. As muscle biopsy revealed non-toxic epithelial cell granulomas, he was diagnosed as muscle sarcoidosis. Even if bilateral hilar lymphadenopathy is not observed, muscle sarcoidosis should be considered in patients developed with hypercalcemia and limb muscle weakness.
A 76-year-old man, who had undergone surgery for esophageal cancer in 2010, presented to our hospital in April 2017 complaining of prolonged slight fever, loss of appetite, and dysphagia. Initial evaluation revealed a paralyzed left vocal cord, slight muscle weakness of the extremities, left facial paralysis, hoarseness, left sternocleidomastoid and trapezius muscle weakness, tongue deviation to the left, and left hypacusia—suggesting a diagnosis of Garcin’s syndrome. Laboratory tests revealed increased white blood cells and C-reactive protein. Cerebrospinal fluid (CSF) analysis showed mild pleocytosis (predominantly polymorphonuclear cells), elevated protein, and low CSF/plasma glucose ratio. CT showed mild clival erosion, with no evidence of carcinoma recurrence. Brain contrast-enhanced MRI showed abnormal clival marrow, enhanced soft tissue and dura matter from the clivus to the atlantoaxial joint, enhanced soft tissue around the left ear canal, multiple cerebral infarctions in the left watershed zones, and left internal carotid stenosis. There was excessive ear wax and inflammation of the left external acoustic meatus but no otorrhea or otalgia. On the basis of his overall presentation, he was diagnosed with atypical skull base osteomyelitis due to external otitis. He was treated with antibiotic treatment that included ceftazidime for the Pseudomonas aeruginosa detected on bacterial cultures. He did not respond to treatment and died approximately 4 months later. Skull base osteomyelitis is thus an important differential diagnosis candidate after finding unilateral, multiple cranial neuropathy, underscoring the importance of prompt treatment when suspected.