Progression of logopenic variant primary progressive aphasia to apraxia and semantic memory deficits.

Background: Due to the nature of neurodegenerative disorders, patients with primary progressive aphasia develop cognitive impairment other than aphasia as the disorder progresses. The progression of logopenic variant primary progressive aphasia (lvPPA), however, has not been well described. In particular, praxic disorders and semantic memory deficits have rarely been reported.

Prognostic value of brain perfusion single-photon emission computed tomography (SPECT) for language recovery in patients with aphasia.

Aim: To determine the prognostic value of brain perfusion single-photon emission computed tomography (SPECT) in patients with aphasia after a stroke.

Methods: Brain perfusion SPECT with 99mTc-ethyl cysteinate dimer (99mTc-ECD) was used in 16 right-handed patients with aphasia after a left-sided cerebrovascular accident (CVA) in the early chronic period after the onset of CVA. The region of interest (ROI) method was used to calculate the relative regional cerebral blood flow (rCBF) in each cerebral lobe, the thalamus, the putamen and the cerebellum as ratios to the count in the left cerebellar hemisphere.

[A case of portal-systemic shunt encephalopathy due to congenital portal vein hypoplasia presenting with abnormal cerebral white matter lesions on the MRI].

A 49-year-old woman, without any past history of liver diseases and blood transfusion, was admitted to our service because of somnolence, and flapping tremor. Neurologically, she was drowsy and disoriented. She had bilateral pyramidal tract signs and flapping tremor.

[A case of Gitelman's syndrome presenting with the hypokalemic periodic paralysis].

We report a rare case of Gitelman's syndrome (GS) presenting with the hypokalemic periodic paralysis. A 27-year-old man was admitted to our hospital because of transient weakness of the limbs. Past history was unremarkable, including the delivery and early developmental milestones, except for a transient limb weakness 7 times since the age of 15 years.

Type-2 astrocyte-like cells are more resistant than oligodendrocyte-like cells against non-N-methyl-D-aspartate glutamate receptor-mediated excitotoxicity.

Glutamate causes excitotoxicity via non-N-methyl-D-aspartate (NMDA) glutamate receptors (GluR) in oligodendrocytes. Because both oligodendrocytes and type 2 astrocytes are differentiated from oligodendrocyte-type 2 astrocyte (O-2A) progenitor cells, we investigated whether astrocytes are also vulnerable to non-NMDA GluR-mediated excitotoxicity. For these studies, oligodendrocyte-like cells (OLC) and type 2 astrocyte-like cells (2ALC) were derived from CG-4 cells, an immortalized rat O-2A progenitor cell line.