Publications by authors named "Takanari Toyoda"

Background: Posterior interosseous neuropathy is an uncommon cause of peripheral dystonia.

Case Report: A 62-year-old man awakened and noticed right finger drop. A neurological examination revealed posterior interosseous neuropathy with dystonia-like finger movements.

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Here we report the first case of phenytoin intoxication that was closely associated with hand-foot synkinesis. This case suggests a close association between cerebellar dysfunction and hand-foot synkinesis. In patients with hand-foot synkinesis, lesions of not only the secondary motor areas but also the cerebellum should be considered.

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Cranial neuropathy is a clinical manifestation of meningeal carcinomatosis (MC); however, the glossopharyngeal and vagus nerves are rarely impaired. Therefore, dysphagia and bilateral vocal cord paralysis (BVCP) are extremely rare manifestations of MC. Here, we present a case of MC from a lung adenocarcinoma presenting with dysphagia and BVCP.

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We report a 44-year-old woman who presented with bilateral weakness of the hands and distal paresthesia of the arms on the next day of the second COVID-19 vaccine, and gradually progressed ascending weakness of the arms and legs, and sensory ataxia beyond 2 months. She was diagnosed as a chronic inflammatory demyelinating polyneuropathy (CIDP) following COVID-19 vaccine on the basis of clinical and electrophysiological findings. This is a first case diagnosed as a CIDP following COVID-19 vaccine alone.

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We herein report the first case of occipital neuralgia secondary to spinal cord infarction. A 74-year-old woman suddenly developed numbness and dysmetria in her right arm. Two days later, she developed a paroxysmal shooting pain in the right posterior part of the scalp three to five times per day.

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We herein report a 74-year-old man who developed Lambert-Eaton myasthenic syndrome (LEMS) during atezolizumab treatment for extensive-stage small-cell lung cancer. He was started on maintenance immunotherapy with atezolizumab every three weeks after four cycles of atezolizumab plus carboplatin plus etoposide combination therapy. After 13 cycles of maintenance atezolizumab therapy, he complained of muscular weakness and fatigue.

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A 41-year-old woman who had been taking paroxetine began taking tramadol for bilateral ankle pain. A few days later, the patient presented acutely with both feet tremors. During a mental arithmetic task, index-finger pointing posture briefly appeared on the left side.

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Ramsay Hunt syndrome (RHS) is an acute peripheral facial nerve paralysis typically accompanied by erythematous vesicular lesions of the auricular skin. The etiology is considered to be geniculate ganglionitis due to reactivation of varicella-zoster virus (VZV). Encephalitis is a rare but serious complication of VZV reactivation.

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IgG4-related disease (IgG4-RD) is a recently recognized disease entity. A 74-year-old male presented with transient headache. He was diagnosed IgG4-RD by pancreatic biopsy at the age of 72.

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We herein report a patient with Miller Fisher syndrome mimicking Tolosa-Hunt syndrome. A 47-year-old man presented with right orbital pain and diplopia. On a neurological examination, he had right oculomotor nerve palsy and diminished deep tendon reflexes.

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Objective: It has been reported that administration of octanoic acid, one of medium-chain fatty acids (MCFAs), promoted leucine oxidation in vitro and in vivo, but it remained unclear how octanoic acid stimulated leucine oxidation. Therefore, the aim of this study was to elucidate the mechanism that octanoic acid facilitates branched-chain amino acid (BCAA) catabolism.

Materials/methods: In in vivo experiments, male rats were orally administered MCFAs as free fatty acids or triacylglycerol (trioctanoin), and then activities of hepatic branched-chain α-ketoacid dehydrogenase (BCKDH) complex (BCKDC) and BCKDH kinase (BDK) and alterations in the concentration of blood components were analyzed.

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Branched-chain α-ketoacid (BCKA) dehydrogenase complex (BCKDC) regulates branched-chain amino acid (BCAA) metabolism at the level of BCKA catabolism. It has been demonstrated that the activity of hepatic BCKDC is markedly decreased in type 2 diabetic animal models. In this study, we examined the regulation of hepatic BCKDC in rats with diet-induced obesity (DIO).

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Hippocampal cholinergic neurostimulating peptide (HCNP) induces the synthesis of acetylcholine in the medial septal nucleus in vitro and in vivo. The precursor, HCNP-pp, is a multifunctional protein participating in important signaling pathways, such as MAPK/ERK kinase (MEK) and G-protein-coupled receptor kinase 2 (GRK2). We recently demonstrated that HCNP-pp colocalizes with collapsin response mediator protein-2 (CRMP-2) at presynaptic terminals in the hippocampus, suggesting that HCNP-pp may play an important role in presynaptic function in association with CRMP-2.

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Hippocampal cholinergic neurostimulating peptide (HCNP) is known to promote differentiation of septohippocampal cholinergic neurons. The HCNP precursor protein (HCNP-pp) may play several roles, for example, as an ATP-binding protein, a Raf kinase inhibitor protein, and a phosphatidylethanolamine-binding protein, as well as a precursor for HCNP. This study therefore aimed to elucidate the involvement of HCNP-pp in specific neural lineages after stroke using a hypoxic-ischemic (HI) rat model of brain ischemia.

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We previously reported a novel peptide, Hippocampal Cholinergic Neurostimulating Peptide (HCNP), which induces acetylcholine synthesis by increasing the amount of choline acetyltransferase (ChAT) in medial septal nuclei. The HCNP precursor protein (HCNP-pp), composed of 186 amino acids, is an inhibitory factor of the c-Raf/MEK cascade and may be involved in fetal rat brain development via the inhibition of phosphorylation of Erk. To clarify the involvement of HCNP in hippocampal cholinergic circuitry, we previously generated HCNP-pp transgenic (HCNP-pp Tg) mice using the promoter of the α subunit of Ca(2+) calmodulin-dependent protein kinase II (CaMKIIα).

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Subthalamic nucleus deep brain stimulation (STN-DBS) is an effective treatment option for medically refractory Parkinson's disease (PD). However, some patients show deterioration of axial symptoms within a short time after surgery. We studied 43 patients who underwent bilateral STN-DBS and investigated predictive factors affecting early deterioration of axial symptoms.

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Hippocampal cholinergic neurostimulating peptide (HCNP), originally purified from young rat hippocampus, has been known to promote the differentiation of septo-hippocampal cholinergic neurons. Recently, the precursor protein of HCNP (HCNP-pp) has also received attention as a multifunctional protein with roles, in addition to serving as the HCNP precursor, such as acting as an ATP-binding protein, a Raf kinase inhibitor protein (RKIP), and phosphatidylethanolamine-binding protein (PEBP). In particular, the function of RKIP has attracted attention over several years for its role in controlling cellular proliferation and metastasis in cancer cells.

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Acetylcholine modulates neural activity in the hippocampal glutamatergic pathway via the induction of phosphorylated Erk and may act as a novel transmitter in septohippocampal memory formation. However, how acetylcholine synthesis in the septal nucleus is regulated is unknown. We have purified a peptide from the hippocampus of the young adult rat, named hippocampal cholinergic neurostimulating peptide (HCNP) that induces acetylcholine synthesis in vitro in the septal nucleus.

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Apraxia of eyelid opening (ALO) is an infrequent side effect of deep brain stimulation (DBS) of the subthalamic nucleus (STN) for Parkinson's disease (PD). However, the pathogenesis of ALO after STN DBS is not well understood. We report on two patients who suffered from disabling ALO after bilateral STN DBS.

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A 79-year-old, bedridden woman with an untreated colon cancer, developed abrupt disturbance of consciousness and high fever. Brain MRI showed significant high signals in the subarachnoid space and ventricles in diffusion-weighted images (DWIs), and she died on the same day. At autopsy, much exudate was found over the base of the brain, leading to a diagnosis of purulent meningitis.

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