A woman in her 30s who was being treated for a mental illness with several psychotropic drugs was admitted to the hospital after being found in a state of unconsciousness and respiratory arrest at home. She was pronounced dead 12 hours after she was discovered. Her autopsy revealed symmetrical hemorrhagic necrosis in the putamen on both sides of her cerebrum. Although many drugs were detected in her blood, all of those other than dextromethorphan (DXM) were within or below the therapeutic range. Her blood DXM was 1.73 μg/ml at admission and 1.61 μg/ml at autopsy, which were within the toxic range or coma-to-death range. The cause of death was diagnosed as DXM poisoning. DXM can cause hallucinations and euphoria if taken in excess, but since it is available as an over-the-counter drug at general pharmacies, an increasing number of young people are overdosing on it, mistakenly believing it to be a safe drug with few side effects. We believe that further social measures against DXM are necessary in Japan, such as disseminating correct knowledge in society and regulating over-the-counter sales.

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This report details the presentation of a 72-year-old female with left-sided continuous non-rhythmic involuntary movements persisting for two months. The movements affected the left side of her face, arm, and leg. The patient had a history of multiple hyperglycemic episodes and diabetic ketoacidosis. This report investigates the basal ganglia\'s involvement in hemiballismus, a movement disorder possibly linked to the patient\'s hyperglycemia. It discusses the complex management of hyperglycemia-induced hemiballismus and the need for more research to understand the underlying mechanism and optimal treatment strategies.

UNASSIGNED: In typical patients with multiple system atrophy with predominant parkinsonism (MSA-P) levodopa is ineffective. However, there are some of these patients who respond well to levodopa treatment. Levodopa efficacy in MSA-P patients is thought to be related to the degree of putaminal damage, but the pathological causation between the putaminal involvement and levodopa efficacy has not been established in detail.
UNASSIGNED: This study aimed to evaluate the neuropathological features of the nigrostriatal dopaminergic system in a \"levodopa-responsive\" MSA-P patient in comparison with \"levodopa-unresponsive\" conventional MSA-P patients.
UNASSIGNED: Clinicopathological findings were assessed in a 53-year-old Japanese man with MSA who presented with asymmetric parkinsonism, levodopa response, and later wearing-off phenomenon. During autopsy, the nigrostriatal pathology of presynaptic and postsynaptic dopaminergic receptor density and α-synuclein status were investigated. The other two patients with MSA-P were examined using the same pathological protocol.
UNASSIGNED: Four years after the onset, the patient died of sudden cardiopulmonary arrest. On autopsy, numerous α-synuclein-positive glial cytoplasmic inclusions in the basal ganglia, pons, and cerebellum were identified. The number of neurons in the putamen and immunoreactivity for dopamine receptors were well-preserved. In contrast, significant neuronal loss and decreased dopamine receptor immunoreactivity in the putamen were observed in the \"levodopa-unresponsive\" MSA-P control patients. These putaminal pathology results were consistent with the findings of premortem magnetic resonance imaging (MRI). All three patients similarly exhibited severe neuronal loss in the substantia nigra and decreased immunoreactivity for dopamine transporter.
UNASSIGNED: Levodopa responsiveness in patients with MSA-P may be corroborated by the normal putamen on MRI and the preserved postsynaptic nigrostriatal dopaminergic system on pathological examination. The results presented in this study may provide a rationale for continuation of levodopa treatment in patients diagnosed with MSA-P.

BACKGROUND: Freezing of gait (FOG) is one of the most debilitating symptoms in patients with idiopathic Parkinson\'s disease (IPD). Visual cues can relieve FOG symptoms. However, there is no consensus on patient characteristics that can benefit from visual cues. Therefore, we examined the differences in IPD patient characteristics according to the effectiveness of visual cueing.
METHODS: Through gait experiments, we investigated the number of FOG occurrences, average FOG period per episode, proportion of FOG duration in the total gait cycles, and FOG-free period gait spatiotemporal parameters in ten participants diagnosed with FOG due to IPD. Subsequently, the differences between their clinical characteristics and striatal dopamine active transporter availability from six subregions of the striatum were compared by dividing them into two groups based on the three reduction rates: occurrence numbers, mean durations per episode, and proportion of FOG duration in the total gait cycles improved by visual cueing using laser shoes. The relationships among these three reduction rates and other FOG-related parameters were also investigated using Spearman correlation analyses.
RESULTS: According to the three FOG-related reduction rates, the group assignments were the same, which was also related to the baseline self-reported FOG severity score (New Freezing of Gait Questionnaire): the more severe the FOG, the poorer the response to the visual cueing. By visual cueing, the better response group demonstrated the characteristics of lower new FOG questionnaire total scores, higher dopamine active transporter availability of the anterior and posterior putamen, and shorter mean duration of FOG per episode in the absence of cueing. These results were replicated using Spearman correlation analyses.
CONCLUSIONS: For FOG symptoms following IPD, gait assistance by visual cueing may be more effective when the total NFOGQ score is lower and the DAT of putamen is higher. Through this study, we demonstrated clinical and striatal dopaminergic conditions to select patients who may be more likely to benefit from visual cueing with laser shoes, and these findings lead to the need for early diagnosis of FOG in patients with IPD.
BACKGROUND: ClinicalTrials.gov identifier: NCT05080413. Registered on September 14, 2021.

We encountered a case of multiple system atrophy parkinsonian subtype (MSA-P) with right-dominant parkinsonism in the early stage of the disease. Atrophy of the posterolateral putamen and iron deposition are the neuropathological hallmark of MSA-P. Coronal fluid-attenuated inversion-recovery (FLAIR) images showed atrophy and iron deposition in the left posterior putamen contralateral to the clinical dominant side in the early phase. Atrophy in the posterior putamen of patients with MSA-P was more clearly observed on coronal FLAIR images than on axial T2-weighted images. These findings reflected the pathological changes and might be a pathognomonic sign of MSA-P.

Autoimmune basal ganglia encephalitis (BGE) typically presents with acute onset parkinsonism and on imaging is associated with lesions in the basal ganglia. It is associated with chorea and other movement disorders. Seizures are still rare. Various autoantibodies are associated with the development of basal ganglia encephalitis. These autoantibodies are against dopamine D2 receptor (D2R) and N-methyl-D-aspartate receptor (NMDAR). Another paraneoplastic antibody known as anti-recoverin antibodies (Abs) is also associated with basal ganglia encephalitis. We report a case of a 45-year-old male who presented in this hospital with a history of cognitive dysfunction and slowness of activities for eight days and faciobrachial seizures. Magnetic resonance imaging (MRI) of the brain revealed lesions in the putamen and caudate nucleus. Infection and antibody screening were negative. The seizures were refractory to conventional antiepileptics. The patient responded to intravenous immunoglobulin (IVIG) therapy.

A 61-year-old man was admitted to our hospital due to cerebral infarction in the pons and the right putamen. On admission (day 3 from symptom onset), laboratory testing showed a white blood cell count of 13,100/μl with hypereosinophilia of 3,734/μl. As deep vein thrombosis was detected on contrast-enhanced CT, we started anticoagulation therapy. There were no cardio-embolic sources, including right-to-left shunt, but eosinophil infiltration was found in biopsy specimens of the gastric mucosa. These findings allowed us to diagnose multiple perforator infarction due to idiopathic hypereosinophilic syndrome (idiopathic HES). After the administration of oral prednisolone was started on day 10, his hypereosinophilia rapidly improved, and no recurrence of deep perforator infarction occurred other than a symptomatic infarction in the left putamen at day 19. There are a few reports of idiopathic HES with multiple infarctions developing in deep perforator regions. The current case suggests that idiopathic HES could cause multiple cerebral infarction restricted to deep perforator areas.