[Intractable Orthostatic Hypotension in Patients with Parkinson's Disease: General Matters about Orthostatic Hypotension and Cautionary Notes through Our Observed Refractory Cases].

Some patients with Parkinson's disease and multiple system atrophy suffer from orthostatic hypotension as a result of cardiovascular autonomic dysfunction. Other complicated dysfunctions, such as spinal hypertension, hinder the management of orthostatic hypotension. A combination of pharmacological and non-pharmacological interventions is required for successful treatment. In this article, I first discuss general matters regarding orthostatic hypotension, after which I describe refractory cases of orthostatic hypotension I have encountered in clinical practice.

Pathologic and Neuropathologic Study of a Case of COVID-19.

A 68-year-old woman with a history of schizophrenia developed coronavirus disease (COVID)-19 and was transferred to our hospital. Despite treatment, she died of respiratory failure 16 days after the onset. At the time of autopsy, polymerase chain reaction (PCR) for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA using swabs from the nasopharynx and the lung was positive; however, the cerebrospinal fluid was negative. An autopsy showed diffuse alveolar damage and recent multiple cerebral infarcts. Acute splenitis was observed with thrombi adhering to the vascular endothelium in areas of severe neutrophilic infiltration. Immunohistochemistry using an antibody against the SARS-CoV-2 nucleocapsid showed immunoreactivity along the hyaline membrane of the lung; however, the antibody showed no immunoreactivity in the medulla, the thalamus, the frontal lobe, and the pituitary. Future pathologic studies should clarify the mechanisms involved in a variety of clinical and pathological changes related to COVID-19.

Propionibacterium acnes-associated chronic hypertrophic pachymeningitis followed by refractory otitis media: a case report.

BACKGROUND: Hypertrophic pachymeningitis (HP) is a rare disorder that involves localized or diffuse thickening of the dura mater. HP is associated with various inflammatory, infectious, and malignant diseases, such as rheumatic arthritis, sarcoidosis, anti-neutrophil cytoplasmic antibody-associated vasculitis, IgG4-related disorders, syphilis, tuberculosis, bacterial and fungal infections, cancer, and idiopathic diseases, when evaluation fails to reveal a cause. Among them, chronic infection with Propionibacterium acnes is a rare etiology of HP, and its pathology remains unclear. CASE PRESENTATION: An 80-year-old man having refractory otitis media with effusion of the right ear presented with progressive right-sided headache and nausea. Post-contrast brain magnetic resonance imaging revealed right mastoiditis and remarkable thickening of the dura mater and enhancement of pia mater extending from the right middle cranial fossa to the temporal lobe. HP secondary to middle ear infection was suspected, and a biopsy of the right mastoid was performed. An anaerobic culture of the biopsied right mastoid showed the growth of P. acnes, and histopathological examination using P. acnes-specific monoclonal antibody (PAB antibody) revealed the infiltration of inflammatory cells with P. acnes. Moreover, using PAB antibody, P. acnes was detected in the biopsy specimen of the thickening dura mater. No granulomas were identified in either specimen. HP was resolved with long-term administration of antibiotics and steroids. CONCLUSION: This is the first documentation of pathologically demonstrated chronic HP associated with P. acnes infection followed by refractory otitis media. This report showed that chronic latent P. acnes infection induces chronic inflammation.

Burst spinal cord stimulation for pain and motor function in Parkinson's disease: A case series.

INTRODUCTION: Spinal cord stimulation (SCS) is an established strategy for pain reduction used in whole world including Japan to treat chronic intractable pain. Pain is a frequent comorbidity of Parkinson's disease (PD), leading to poorer quality of life. SCS has been reported to effectively reduce pain in PD and may also improve motor function, but most studies have employed the modality of tonic stimulation. As such, the effects of SCS using the newly developed paradigm of burst stimulation in PD remain relatively unexplored. METHODS: This case series reviewed PD patients who underwent SCS using BurstDR stimulation to treat intractable lower back pain (LBP). Pain and motor outcomes were assessed before and at several timepoints after implantation over a 24-week observation period. RESULTS: Pain indices (visual analogue scale [VAS] and short-form McGill Pain Questionnaire 2 [SF-MPQ-2] scores) improved in nearly all patients. Improvements were especially notable in the dimension of affective pain (SF-MPQ-2). Functional motor improvements were evident in the Unified Parkinson's Disease Rating Scale (UPDRS), especially walking-related items, and timed-up-and-go (TUG) test performance, which generally persisted through week 24 of observation. CONCLUSION: Burst SCS improved pain (especially the affective component) in PD patients with LBP, with effects generally lasting for at least 24 weeks. Neither paresthesia nor obvious adverse events were experienced in any case. Motor symptoms as scored of UPDRS Part III had the trends of improvement in lower limb akinesia at week 24 and gait at week 4. These findings suggest that burst SCS may be an effective treatment option for LBP and may be influenced to gait-related motor symptoms in PD.

Late-onset paradoxical reactions 10 years after treatment for tuberculous meningitis in an HIV-negative patient: a case report.

BACKGROUND: Although paradoxical reactions (PRs) to anti-tuberculosis (anti-TB) therapy during treatment are well-established occurrences, PRs presenting as a new lesion after the completion of treatment are extremely rare, and little is known about the management of such cases, particularly of central nervous system (CNS) tuberculosis. CASE PRESENTATION: A 27-year-old female, with a past medical history of tuberculous meningitis 10 years ago and who completed the anti-TB treatment with asymptomatic remnant tuberculomas in the basal cistern, was admitted to our hospital because of a headache and the worsening of pre-existing visual disturbance. Contrast-enhanced T1-weighted brain magnetic resonance imaging (MRI) revealed new tuberculomas in the left sylvian fissure with a diffuse low signal around it. Because repeated polymerase chain reaction and Mycobacterium tuberculosis culture presented negative results and the patient had no laboratory data suggestive of a relapse of tuberculous meningitis, she was diagnosed with late-onset post-treatment PRs and treated with oral corticosteroids, tapered off over 1 year. Eventually, the symptoms were relieved, and the tuberculomas disappeared. CONCLUSIONS: Clinicians should consider the possibility of PRs long after the completion of tuberculous meningitis treatment. Hence, a precise MRI-based examination is imperative for the follow-up of CNS tuberculosis, and the unnecessary administration of anti-TB drugs should be avoided. The use of corticosteroids as a treatment option for post-treatment PRs is seemingly safe when the isolated M. tuberculosis is sensitive to the first-line anti-TB therapy.

Syringomyelia due to Lumbar Spinal Fluid Drainage in the Acute Phase of Subarachnoid Hemorrhage: A Case Report.

Lumbar spinal fluid drainage is a common procedure for treating hydrocephalus and alleviating vasospasm by egesting blood in the subarachnoid cavity after subarachnoid hemorrhage. Despite being an effective and safe procedure, cerebrospinal fluid overdrainage might result in serious complications. Here we report the case of a 49-year-old man who suffered from tonsillar herniation with subsequent cervicothoracic syringomyelia in the acute phase of subarachnoid hemorrhage due to vertebral artery dissection. About 2 weeks after lumbar drainage was switched from external ventricular drainage initiated on the day of subarachnoid hemorrhage, the recovery from the disturbance of consciousness revealed tetraplegia, and magnetic resonance imaging demonstrated tonsillar herniation and syringomyelia. Removal of the spinal drain and resumption of external ventricular drainage resulted in the restoration of the herniated tonsils to the normal position and the complete disappearance of syringomyelia 11 days later. We should consider that spinal syringomyelia could develop as a complication of lumbar spinal fluid drainage in the acute phase of thick subarachnoid hemorrhage, particularly in the posterior cranial fossa.

Pitfalls in the diagnosis of pupil-sparing oculomotor nerve palsy without limb ataxia: A case report of a variant of Claude's syndrome and neuroanatomical analysis using diffusion-tensor imaging.

Midbrain infarction causing oculomotor nerve palsy with contralateral ataxia is named Claude's syndrome. Herein we report the case of a variant of Claude's syndrome, which shows pupil-sparing oculomotor nerve palsy without the accompanying neurological deficits other than subtle truncal ataxia. MRI and Diffusion Tensor Imaging revealed that midbrain infarction was located rostrally above the decussation of the superior cerebellar peduncle (SCP) and might have partially destructed the tectospinal tract, which resulted in the absence of limb ataxia and presence of subtle truncal ataxia. In this variant of Claude's syndrome, we should carefully assess truncal ataxia to avoid misdiagnosing it as isolated pupil-sparing oculomotor nerve palsy because the patient showed apparently normal gait and truncal ataxia was only revealed by unstable tandem gait.