The underlying pathophysiology of slight cognitive dysfunction in Parkinson’s disease-related mild cognitive impairment (PD-MCI) is yet to be elucidated. Our study aimed to evaluate the association between cognitive function and brain functional connectivity (FC) in patients with PD-MCI. Twenty patients with sporadic PD-MCI were evaluated for FC in the brain network. Further, electroencephalography (EEG) coherence analysis in the whole-brain and quantified regional coherence using phase coupling were performed for each frequency, and motor and cognitive function were assessed in the whole-brain. The degree of cognitive impairment was related to a decrease in the coherence in the alpha ranges. The regional coherence in the left frontal-left parietal region rather than the right frontal-right parietal region showed a higher correlation with the cognitive function scores. The differences in EEG coherence across different types of cognitive dysfunction reflect a compensatory response to the heterogeneous and complex clinical presentation of PD-MCI. Our findings indicate decreased brain efficiency and impaired neural synchronization in PD-MCI; these results may be crucial in elucidating the pathological exacerbation of PD-MCI.

Patients with Parkinson’s disease (PD) often experience pain, which fluctuates in “on” and “off” states, but the underlying mechanism is unclear. The nucleus accumbens (NAc) is a central component of the mesolimbic dopaminergic pathway involved in pain processing. We conducted resting-state functional magnetic resonance imaging (rsfMRI) analysis to explore the relationship between the neuronal synchronization of NAc with pain-related brain regions and pain intensity in “on” and “off” states. We assessed 23 patients with sporadic PD based on rsfMRI and pain intensity using the revised Short-Form McGill Pain Questionnaire. Patients with PD displayed higher pain intensity scores in the “off” state than in the “on” state. The pain intensity in the “off” state was substantially correlated with the functional connectivity (FC) between the NAc and primary motor/sensory cortices and contralateral NAc. Changes in pain intensity from the “on” to “off” state displayed correlations with those between the right (rNA) and left NAc (lNAc) and the right precentral gyrus (rPreCG) /right insular cortex (rIC) from the “off” to “on” state. Aberrant bilateral NAc and rNAc–rPreCG/rIC FC in the “off” state were closely related to pain symptoms developed from the “on” to “off” states. These results suggest that the NAc in the mesolimbic pathway is related to pain in PD and may help understand the mechanism of pain development in patients with PD.

Repetitive transcranial magnetic stimulation (rTMS) is reportedly a potential tool to understand the neural network; however, the pathophysiological mechanisms underlying cognitive function change remain unclear. This study aimed to explore the cognitive function changes by rTMS over the bilateral dorsolateral prefrontal cortex (DLPFC) in Alzheimer’s disease (AD). We evaluated the feasibility of rTMS application for mild cognitive dysfunction in patients with AD in an open-label trial (UMIN000027013). An rTMS session involved 15 trains at 120% resting motor threshold on each side (40 pulses/train at 10 Hz). Efficacy outcome measures were changes from baseline in cognitive function, assessed based on the AD Assessment Scale-cognitive subscale, Mini-Mental State Examination, Japanese version of Montreal Cognitive Assessment (MoCA-J), Behavioral and Psychological Symptom of Dementia, and Instrumental Activity of Daily Living scores. Sixteen patients with AD underwent five daily sessions of high-frequency rTMS over the bilateral DLPFC for 2 weeks. All participants completed the study; no major adverse effects were recorded. The MoCA-J score increased by 1.4 points (±0.15%) following 2 weeks of stimulation. At 1 month following rTMS cessation, all cognitive functional scores returned to the original state. Our findings suggest that the DLPFC plays an important role in the neural network in AD.

Objective: To evaluate the usefulness of thoracic excursion as a biomarker in patients with amyotrophic lateral sclerosis (ALS).Methods: We measured the forced the vital capacity (FVC), thoracic excursion, baseline-to-peak diaphragmatic compound muscle action potential (DCMAP) amplitude, diaphragm thickness at full inspiration (DTfi), Medical Research Council (MRC) sum score for muscle strength, and arterial partial pressures of oxygen and carbon dioxide and administered the Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) and modified Medical Research Council (mMRC) Dyspnea Scale. The test–retest reliability of thoracic excursion was determined.Results and Conclusions: Thirty-four patients with ALS and 26 age- and sex-matched healthy participants were enrolled. Thoracic excursion measurement had excellent test–retest reliability (intraclass coefficient: 0.974). Thoracic excursion was more strongly correlated with FVC (r = 0.678, p < 0.001) than DCMAP amplitude (r = 0.501, p = 0.003) and DTfi (r = 0.597, p < 0.001). It was also correlated with ALSFRS-R score (r = 0.610, p < 0.001), MRC sum score (r = 0.470, p = 0.005), and mMRC Dyspnea Scale score (r = −0.446, p = 0.008) and was the most sensitive parameter for assessing dyspnea and FVC. Thoracic excursion decreased as FVC declined in the early and late stages, there were no differences in DCMAP amplitude and DTfi between the early and late stages, and ALSFRS-R score and MRC sum score decreased only in the late stage. Thoracic excursion was well correlated with respiratory function and is useful for predicting respiratory and general dysfunction in patients with ALS regardless of stage.

The present report highlights a case of successful treatment of an 11-year-old male patient who presented with an atlanto-occipital dislocation and multiple fractures of the forearm, pelvis, and lower leg because of a fall. The patient experienced dysarthria and paralysis of the tongue, which became completely immobile and could not be moved from side to side, impeding speech. The patient also experienced dysphagia due to the inability to propel food toward the pharynx and chewing attempts resulted in scattering of food residue throughout the oral cavity. The lack of tongue mobility led to saliva accumulation, forcing the patient to swallow frequently, which was possible as larynx movement was unaffected. The other cranial and motor sensory nerves appeared normal. Our diagnostic examinations confirmed the presence of isolated bilateral paralysis of the hypoglossal nerve secondary to traction at the base of the skull. The patient was still unable to protrude his tongue and tongue gradually atrophied two weeks after admission. Electromyography revealed denervation of the tongue and minimal active contraction of the single motor units. Immobilization therapy and rehabilitation therapy were initiated to improve tongue movement, but this was unsuccessful and one month after the accident, the patient's tongue was still atrophied. The patient was placed on a soft food diet and experienced no difficulty in swallowing either saliva or food three months after admission. Tongue mobility was deemed normal. Electromyography six months after the initial episode revealed normal motor unit potentials during contractions. We postulate that compression and stretching of the bilateral hypoglossal nerves against the greater horn of the hyoid bone was a probable cause of the hypoglossal palsy. The use of immobilization and rehabilitation therapy likely supported the recovery of functionality and resulted in a good prognosis.