Early-onset Cervical Myelitis after COVID-19 Vaccination.

A 33-year-old woman developed paresthesia in her right thumb approximately 30 minutes after receiving the BNT162b2 (Pfizer-BioNTech) severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine. The paresthesia gradually spread to her right-side limbs and trunk, and cervical magnetic resonance imaging (MRI) revealed a localized lesion in the right dorsal column. After glucocorticoid therapy, her symptoms and MRI findings improved. Although disease developing less than 24 hours after vaccination is considered an unlikely cause of immuno-associated adverse events following vaccination, we discuss the possible mechanisms involved in early-onset central nervous system inflammation after vaccination in view of preexisting immunopathological susceptibility.

[A case of primary central nervous system lymphoma with marked cauda equina enlargement].

An 80-year-old woman presented with subacute right lower limb pain and bilateral lower limb weakness. MRI of the spine showed marked cauda equina enlargement with contrast enhancement. Cerebrospinal fluid (CSF) examination showed elevated cell count, decreased glucose, and elevated protein. Cytology of the CSF showed class V, which together with B-cell clonality by flow cytometry, led to the diagnosis of primary central nervous system lymphoma (PCNSL). The patient was treated with steroid, radiation, and chemotherapy. Despite the reduction in lesion size, her neurological symptoms revealed no improvement. PCNSL with cauda equina lesions are rare and often require highly invasive cauda equina biopsy for diagnosis. In recent years, some studies reported useful CSF biomarkers, but they may have some problems. Therefore, as in this case, the combination of cytology, flow cytometry and, CSF biomarkers could be a substitute method for invasive biopsies, and contribute to the early treatment of PCNSL.

Pathologically Proven Gadolinium-enhanced MRI Lesions in the Bilateral Corticospinal Tracts in Lymphomatosis Cerebri.

A 78-year-old woman in complete remission of mass-forming primary central nervous system lymphoma (PCNSL) showed diffuse leukoencephalopathy as well as corticospinal tract lesions with intense gadolinium enhancement on magnetic resonance imaging (MRI). She died 3 months later. In line with the MRI findings, pathological examination revealed dense infiltration of atypical lymphoid cells, consistent with a diagnosis of lymphomatosis cerebri (LC)-type PCNSL. This is the first report of LC in which the corticospinal tracts demonstrated robust contrast enhancement directly corresponding to the neuropathological findings, and it is also a rare instance in which LC presented as a recurrence of typical PCNSL.

[Foix-Chavany-Marie Syndrome: A Clinical Overview].

Foix-Chavany-Marie syndrome, which has been reported since the 19th century, is a cortical type of pseudobulbar palsy. Although previously most cases were due to acute recurrent stroke, recent reports have indicated that there are various causes, including infectious, developmental, epileptic and degenerative processes and various clinical courses, which may be transient or slowly progressive. Moreover, modern imaging techniques have revealed the significance of the injury of the white matter tract, such as the frontal aslant tract, rather than classical lesions of bilateral motor cortices. Considering both the findings of the bedside examination of patients with this "old" syndrome and of "new" imaging studies performed at appropriate times is expected to contribute to our understanding of the neural underpinnings of this syndrome.

Statokinetic Dissociation (Riddoch Phenomenon) in a Patient with Homonymous Hemianopsia as the First Sign of Posterior Cortical Atrophy.

We report a 60-year-old woman with posterior cortical atrophy (PCA) who presented with left homonymous hemianopsia persisting for 5 years; the patient's condition was observed using static, but not kinetic, perimetry. This statokinetic dissociation of hemianopsia, which is often called Riddoch syndrome, might have been caused by a dysfunction of the right primary visual and visual association cortices, representing a functional imbalance within a disturbed visual cortex. In patients with PCA and visual field defects, both static and kinetic perimetry may be useful for understanding the extent of degeneration in the visual cortex, in addition to examinations of unilateral neglect.

Diffuse Leukoencephalopathy Associated with Dialysis Disequilibrium Syndrome.

A 52-year-old woman, previously treated for gastric cancer, began hemodialysis (HD) to treat the onset of severe acidemia. After her initial HD sessions, she suffered from a prolonged coma for approximately ten days. Magnetic resonance imaging revealed diffuse leukoencephalopathy, with increased apparent diffusion coefficient. Magnetic resonance spectroscopy showed a reduction of the N-acetylaspartate/creatine ratio. Her neuroimaging findings gradually resolved. Her transient cerebral white matter lesions were thought to be interstitial edema derived from dialysis disequilibrium syndrome (DDS), which might have been amplified by subclinical brain injury due to past chemotherapy. Her history of cancer chemotherapy may be a risk factor for an exacerbation of DDS.

Guillain-Barré syndrome variant with facial diplegia and paresthesias associated with IgM anti-GalNAc-GD1a antibodies.

We herein report the case of a 19-year-old woman with facial diplegia and paresthesias (FDP) preceded by flu-like symptoms. We diagnosed the patient with a regional variant of Guillain-Barré syndrome due to decreased tendon reflexes, albuminocytological dissociation in the cerebrospinal fluid and demyelinating features on nerve conduction studies. The patient also had IgM anti-GalNAc-GD1a antibodies, and treatment with glucocorticoids was effective for treating the facial diplegia, but not paresthesia. Therefore, facial palsy may have a different pathophysiology from paresthesia or other symptoms of FDP, which responds to glucocorticoid therapy.

Room tilt illusion in Parkinson's disease: loss of spatial reference frames?

Room tilt illusion, a misperception that the entire room is tilted, is a rare but nonspecific neurological symptom. We report a patient with Parkinson's disease who developed typical room tilt illusion. Single photon emission computed tomography demonstrated hypoperfusion of the posterior area of the right intraparietal sulcus, which is related to discriminating the surface orientation of three-dimensional objects. Therefore, it is possible that dysfunction of this region of the intraparietal sulcus may have disrupted the integration of spatial reference frames for internal representation of the surrounding space in our patient, and thus may have caused room tilt illusion.

Convergence substitution in pontine tegmental hemorrhage: an observation with Frenzel goggles.

We report a case in which convergence movement was substituted for bilateral horizontal gaze palsy due to a pontine tegmental hemorrhage. When visual fixation was suppressed with Frenzel goggles (FG), substituted convergence movements were prominent in our patient. The observation suggests that both vergence eye movements and horizontal gaze movements act synergistically and lesioning of the version system results in overactivity of the convergence system after a pontine hemorrhage. Furthermore, it may be worth using FG in the observation of substituted eye movements in patients with horizontal gaze palsy due to a pontine tegmental injury.

[Amnesia, confabulation and nonaphasic misnaming after left thalamic infarct].

A 72-year-old right handed woman developed amnesia, confabulation and abnormal (bizarre) verbal response after the left thalamic infarction. Clinical features including disorientation, euphoria and various kinds of paraphasia coincided in nonaphasic misnaming. MR images showed that lesions involved the genu of the internal capsule, the anteroventral nucleus, the lateroventral nucleus, intralaminar nuclei, the mamillothalamic tract and the region around the ventral thalamus. 99mTc-HMPAO-SPECT revealed decreased uptake in the left frontal lobe, probably due to the disconnection from the thalamus. These findings suggest that the dysfunction of the thalamus (mainly ventrolateral) and the left frontal lobe caused the disturbance of the self-monitoring in the language use, which generated confabulation and nonaphasic misnaming in our case.