Recurrent Ipsilateral C5 Nerve Palsy Associated With Hereditary Neuropathy With Liability to Pressure Palsy.

Hereditary neuropathy with liability to pressure palsy (HNPP) is an autosomal dominant disorder caused by heteroplasmic deletion of the peripheral myelin protein 22 (PMP22) gene. HNPP typically presents with clinical features such as peroneal nerve palsy or cubital tunnel syndrome, which are caused by mechanical compression. Diagnosing cases where neuropathy is absent at the pressure site can be challenging. This is a case study of an 18-year-old man who underwent surgery on the left side of his neck over 10 years ago to remove lymphadenopathy. Following the surgery, he experienced recurrent weakness but only sought medical attention when muscle weakness persisted for longer than a week postoperatively. Upon admission, the patient exhibited neurological symptoms consistent with C5 neuropathy, mainly affecting the deltoid muscles. No serological abnormalities were found to be associated with neuropathy. Neither magnetic resonance imaging nor computed tomography scans detected any lesions around the C5 nerve root. The posture during sleep was believed to cause excessive extension of the C5 nerve root, leading to the assumption that there was some vulnerability in the nerve. A transient sensory loss in the area innervated by the ulnar nerve prompted us to examine the fluorescence in situ hybridization study on the blood sample, which revealed a deletion of the PMP22 gene. The patient was diagnosed with HNPP and was advised to avoid risky postures. Following the implementation of these lifestyle changes, he did not experience any further weakness in his shoulders.

Enteral tube nutrition for geriatric post-stroke dysphagia evaluation (ENGE) score to evaluate the risk of dysphagia after acute ischemic stroke.

BACKGROUND: Post-stroke dysphagia (PSD) is a common complication after stroke. Early PSD prediction is essential for patient stratification for intensive oral intake rehabilitation. We aimed to develop a PSD prediction score using clinical data obtained at admission. METHODS: We examined consecutive patients with acute ischemic stroke between 2018 and 2019. The dysphagia status 14 days after admission was assessed using the Functional Oral Intake Scale (FOIS). PSD was defined as FOIS 1-3, which represents tube-dependent nutrition. Using multivariable logistic regression analysis, we constructed the Enteral tube Nutrition for Geriatric post-stroke dysphagia Evaluation (ENGE) score. The discriminative performance of the ENGE score was analyzed by receiver operating curve analysis. The reproducibility of the ENGE score was validated using patient data in 2020. RESULTS: PSD developed in 84 of 488 patients (median age 78 years; 57% males). The ENGE score ranged from 0 to 6, with 1 point assigned for older age (≥78 years), 1 for high premorbid modified Rankin Scale (mRS) (≥1), 3 for high NIHSS score (≥12), and 1 for low serum albumin (<3.0 mg/dl). The area under the curve (AUC) of the ENGE score for discriminating PSD was 0.88 (95% confidence interval [CI] 0.83-0.92), and a score of 3 or more had a higher positive likelihood ratio. In the validation cohort, the AUC of the ENGE score for PSD was 0.85 (95% CI 0.78-0.91), which was similar to the derivation cohort (p = 0.491). CONCLUSIONS: The ENGE score predicts severe PSD after acute ischemic stroke with good reproducibility.

Eustachian Valve-Enhanced Paradoxical Cerebral Embolism: A Case Report.

Cryptogenic stroke includes many suspicious embolic causes that do not fulfill the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification criteria. Atrial fibrillation (AF) is one of the major hidden causes of cryptogenic stroke, and an implantable loop recorder (ILR) is widely used for detecting AF. Herein, we report a case of paradoxical cerebral embolism due to a large Eustachian valve with large PFO under no molecular complete remission (CR) of acute monocytic leukemia (AMoL). A 75-year-old man arrived at our emergency room because of aphasia and right hemiparesis. He had a history of two cryptogenic strokes and implanted ILR. Magnetic resonance imaging showed left middle cerebral artery occlusion with slight acute ischemic lesion. The red clot was retrieved by mechanical thrombectomy, and complete recanalization was achieved. We checked ILR, but there was no AF. Transesophageal echocardiography revealed a large patent foramen ovale (PFO) and the large Eustachian valve in the right atrium. Although obvious deep vein thrombosis (DVT) was not detected in venous ultrasonography of the lower extremities, Wilms' tumor 1 messenger ribonucleic acid (WT1mRNA) expression level was high, and AMoL was considered to be not in molecular CR, suggesting a high risk of thrombosis to the large Eustachian valve. From large PFO and no molecular CR of AMoL, we diagnosed him with paradoxical cerebral embolism. Ruling out of AF by ILR and other etiologies, such as aortic or carotid atherosclerosis and pulmonary shunt, also supported the diagnosis of paradoxical cerebral embolism. Even in the absence of obvious DVT, paradoxical cerebral embolism should be considered in cases of a large Eustachian valve and PFO with a hypercoagulable state.

Geriatric nutrition risk index predicts prolonged post-stroke dysphagia in acute ischemic stroke.

BACKGROUND: Post-stroke dysphagia (PSD) is a common complication after stroke. Malnutrition inhibits stroke recovery and is associated with stroke mortality. However, no studies have investigated the effects of nutritional state at admission on prolonged PSD. METHODS: We retrospectively analyzed ischemic stroke patients in our institute from January 2018 to December 2020. Swallowing function was assessed using the Food Oral Intake Scale; prolonged PSD was defined as levels 1-3 at 14 days after admission. The Geriatric Nutritional Risk Index (GNRI) was used to assess nutritional risks, which were classified as follows: >98, no nutritional risk; 92-98, mild nutritional risk; 82-92, moderate nutritional risk; and <82, severe nutritional risk. The association between GNRI and prolonged PSD was assessed. RESULTS: Of 580 patients (median age, 81 years; male, 53%), prolonged PSD was detected in 117 patients. Patients with severe dysphagia had older age, higher pre-stroke modified Rankin Scale score, lower GNRI, and higher National Institutes of Health Stroke Scale score. Logistic regression analysis revealed that lower GNRI was independently associated with prolonged PSD (continuous value; adjusted odds ratio [OR] 1.03, 95% confidence interval [CI] 1.00-1.05). In addition, when "severe" and "moderate" nutritional risk was analyzed as a single class, moderate or severe nutritional risk (GNRI < 92) was independently associated with prolonged PSD (adjusted OR 2.50, 95% CI 1.29-4.87), compared with no nutritional risk patients (GNRI > 98). CONCLUSIONS: In acute ischemic stroke, lower GNRI at admission was independently associated with prolonged PSD, suggesting that GNRI at admission might identify patients at risk of prolonged PSD.