We propose a new object packing approach, RePack, to arrange a series of identical image objects to a rectangular canvas densely by a deep CNN with reinforcement learning. In our approach, adding a new object to an image pack of existing objects is modeled as classification of possible pack configurations by a CNN. To iteratively reinforce the CNN, pack trees are built to identify object overlaps and to find denser pack configurations for reinforcement training. Such a reinforcement learning process for enhancing a CNN for dense object packing is rarely seen in previous literature. Preliminary experimental results show that the reinforced deep CNN can generate dense object packs in a sequential manner for circular, triangular and quadrilateral objects.

Peripheral facial palsy is often attributed to idiopathic Bell’s palsy, but secondary structural causes should be considered when local red flags are present. A 61-year-old man with a 40-pack-year smoking history and former betel quid chewing presented with a verrucous-appearing mass involving the left oral commissure and buccal mucosa, intermittent purulent discharge from the lesion, progressive left facial swelling, and ipsilateral lower-motor-neuron facial palsy with lagophthalmos. Magnetic resonance imaging demonstrated a left buccal/oral-cavity lesion with ipsilateral parotid duct obstruction. He underwent tracheostomy, wide excision, left supraomohyoid neck dissection, and radial forearm free-flap reconstruction. Pathology confirmed squamous cell carcinoma, pT2N0, cM0 (stage II), with perineural invasion; surgical margins were negative, and lymphovascular invasion was not identified. At follow-up, wound healing was satisfactory and purulent discharge had resolved, but lower-motor-neuron facial palsy persisted; adjuvant radiotherapy was recommended. This case emphasizes that lower-motor-neuron facial palsy with an oral mass, purulent discharge, facial swelling, or salivary-duct obstruction should prompt careful oral examination and head-and-neck imaging.

There is no online version at this time. The PDF is only available to people who have bought the paper or have a subscription.

Background: Persistent depressed consciousness in severe coronavirus disease 2019 (COVID-19) is commonly attributed to hypoxemia, systemic inflammation, sedative exposure, or metabolic disturbance. Non-convulsive status epilepticus (NCSE), however, may be overlooked without electroencephalography (EEG). This diagnostic principle also applies to persistent unexplained encephalopathy more broadly, particularly when impaired consciousness remains disproportionate to systemic illness. Case: An 85-year-old woman with Parkinsonism, diabetes mellitus, and prior cerebrovascular disease developed severe COVID-19 pneumonia followed by persistent coma during intensive care. Brain computed tomography showed chronic atrophic change without acute structural lesions, and laboratory and cerebrospinal fluid findings did not identify a major alternative explanation for coma. On the day of EEG, arterial blood gas analysis showed adequate oxygenation without hypercapnia. EEG on hospital day 10 demonstrated abundant right-hemispheric rhythmic/periodic discharges at approximately 2 Hz and focal electrographic seizures arising from the right temporal region with spatiotemporal evolution, consistent with NCSE. Levetiracetam, lacosamide, and midazolam infusion were administered. Outcome: Midazolam infusion was followed by electrographic seizure resolution but did not produce immediate clinical awakening during sedation; spontaneous eye opening emerged approximately 4 days later. Follow-up EEG on hospital day 13 showed seizure resolution with residual diffuse slowing and a sporadic right-hemispheric spike. Conclusion: This case highlights early EEG as a practical diagnostic and treatment-monitoring tool in severe COVID-19-associated encephalopathy when depressed consciousness is persistent or disproportionate to systemic illness. More generally, EEG should be considered in persistent unexplained coma or encephalopathy after stabilization of cardiopulmonary factors.

Background: Longitudinally extensive transverse myelitis (LETM) is often investigated as an autoimmune inflammatory myelopathy, but treatable infectious mimics should also be considered. Neurosyphilis-associated myelitis is uncommon and may resemble aquaporin-4 or myelin oligodendrocyte glycoprotein antibody-associated disease. Case presentation: A 31-year-old man presented with a one-month history of progressive bilateral lower-limb thermal dysesthesia and hyperesthesia, proximal leg weakness, pyramidal signs, urinary retention, and fecal incontinence. Spinal magnetic resonance imaging showed a longitudinally extensive central thoracic cord T2 hyperintensity from T6 to T10. Serum syphilis serology and cerebrospinal fluid Venereal Disease Research Laboratory testing were reactive, whereas human immunodeficiency virus testing was negative, serum aquaporin-4 and serum myelin oligodendrocyte glycoprotein antibodies were negative, and oligoclonal bands were absent. Because the initial cerebrospinal fluid sample was blood-contaminated and showed no pleocytosis, the diagnosis was considered probable neurosyphilis-associated LETM rather than definitive syphilitic myelitis. The patient received ceftriaxone-based anti-treponemal therapy with adjunctive corticosteroids. Follow-up cerebrospinal fluid Venereal Disease Research Laboratory testing became non-reactive, spontaneous voiding recovered, and follow-up spinal magnetic resonance imaging showed radiologic resolution. Conclusions: Probable neurosyphilis-associated LETM can mimic seronegative inflammatory myelitis. Syphilis testing should be considered early in LETM, particularly when prominent sphincter dysfunction is present. Diagnostic certainty may be limited by atypical cerebrospinal fluid findings, blood contamination, and concomitant antimicrobial and corticosteroid treatment.

Anti-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) encephalitis is a rare, often paraneoplastic, cause of limbic encephalitis. The concurrent presentation of anti-AMPAR encephalitis alongside multiple autoimmune syndromes and antibodies is exceedingly uncommon. We describe a 62-year-old man with no significant past medical history who presented with a rapidly progressive 4-month history of cognitive decline and gait disturbance. Comprehensive evaluation revealed anti-AMPAR encephalitis, thymoma, subclinical myasthenia gravis, and autoimmune thyroiditis, demonstrating coexistence of multiple autoimmune disorders. Immunological assessment identified a complex polyspecific autoantibody profile, including anti-AMPAR2, anti-Titin, anti-glutamic acid decarboxylase 65, anti-anti-acetylcholine receptor, and anti-thyroid antibodies. Following aggressive immunotherapy and thymectomy, the patient experienced substantial neurological improvement. Anti-AMPAR encephalitis can coexist with multiple autoimmune disorders and diverse autoantibodies. Therefore, thorough antibody screening and tumor evaluation are essential to identify occult etiologies and to guide optimal therapeutic strategies.