K Nagasawa

Publications (5)7.97 Total impact

• Article: Empty sella in children as a key for diagnosis.

  J Takanashi, H Suzuki, K Nagasawa, K Kobayashi, N Saeki, Y Kohno
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  ABSTRACT: We performed magnetic resonance imaging of the pituitary gland in 354 children who were under the care of our pediatric neurological outpatient department. Among them, an empty sella was recognized in 11 children, who all showed normal hormonal results. The frequency of an empty sella was significantly high in idiopathic intracranial hypertension (4/4; P<0.0001) and nevoid basal cell carcinoma syndrome (3/5; P<0.0001). The ratio of an empty sella in children, excluding patients with idiopathic intracranial hypertension and nevoid basal cell carcinoma syndrome, is estimated to be 4/345 (1.2%), which is markedly lower than that in adults. Magnetic resonance imaging of the pituitary gland in children could provide important clues for the diagnosis of idiopathic intracranial hypertension or nevoid basal cell carcinoma syndrome.
  Brain and Development 10/2001; 23(6):422-3. · 2.12 Impact Factor
• Article: [Four cases of reversible posterior leukoencephalopathy syndrome].

  M Tomita, J Takanashi, K Kobayashi, K Nagasawa, A Kurihara, K Okumura, T Maemoto, J Ono, Y Kohno
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  ABSTRACT: We reported four children cases with reversible posterior leukoencephalopathy syndrome (RPLS). Magnetic resonance imaging (MRI) of the brain demonstrated reversible multiple cortical and subcortical lesions predominant in the occipital region. All patients presented with neurological symptoms associated with hypertension, such as headache, seizures and visual disturbances, which were successfully treated with antihypertensive therapy. Although RPLS is rare in childhood, characteristic lesions on MRI in the hypertensive children should be recognized as manifestations of RPLS. Subsequent clinical management should focus on the treatment of the hypertension and/or its underlying causes.
  No to hattatsu. Brain and development 10/2001; 33(5):426-9.
• Article: [Clinical and MRI findings in childhood idiopathic intracranial hypertension].

  H Suzuki, J Takanashi, K Nagasawa, K Kobayashi, M Tomita, K Tamai, Y Kohno
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  ABSTRACT: We report here clinical and MRI findings of four children with idiopathic intracranial hypertension (IIH). Their chief complaint was headache. Three patients had papilloedema, and the other one showed the highest cerebrospinal fluid pressure (106 cm H2O) without papilloedema. In two cases, the symptoms disappeared after repeated lumbar punctures. At admission, MRI demonstrated empty sella in all the four cases. Regarding the optic nerves, there were more than two of the following three findings: distension of the perioptic subarachnoid space, vertical tortuosity and elongation of the optic nerve, and flattening of the posterior aspect of the globe. Follow-up MRI showed normalization of sella turtica and/or optic nerve findings in two of the three cases examined. MRI focusing on the optic nerves and pituitary gland may provide important clues for the diagnosis of IIH, especially those without papilloedema.
  No to hattatsu. Brain and development 08/2001; 33(4):319-22.
• Article: MR imaging of idiopathic intracranial hypertension.

  H Suzuki, J Takanashi, K Kobayashi, K Nagasawa, K Tashima, Y Kohno
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  ABSTRACT: We report the case of a 9-year-old male patient with idiopathic intracranial hypertension without papilledema for which MR imaging of the optic nerves and pituitary gland provided important clues for the diagnosis of idiopathic intracranial hypertension and showed a return to normal appearance after normalization of CSF pressure.
  American Journal of Neuroradiology 02/2001; 22(1):196-9. · 2.93 Impact Factor
• Article: MR-revealed myelination in the cerebral corticospinal tract as a marker for Pelizaeus-Merzbacher's disease with proteolipid protein gene duplication.

  J Takanashi, K Sugita, Y Tanabe, K Nagasawa, K Inoue, H Osaka, Y Kohno
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  ABSTRACT: Pelizaeus-Merzbacher's disease (PMD) is caused by mutations in the proteolipid protein (PLP) gene. Recent studies have shown that an increased PLP dosage, resulting from total duplication of the PLP gene, invariably causes the classic form of PMD. The purpose of this study was to compare the MR findings of PMD attributable to PLP duplication with those of PMD arising from a missense mutation. Seven patients with PMD, three with a PLP missense mutation in either exon 2 or 5 (patients 1-3), and four with PLP duplication (patient 4 having larger PLP duplication than patients 5-7) were clinically classified as having either the classic or connatal form of PMD. Cerebral MR images were obtained to analyze the presence of myelination and T1 and T2 shortening in the deep gray matter. Multiple MR studies were performed in six of the seven patients to analyze longitudinal changes. Four patients (patients 1-4) were classified as having connatal PMD, whereas the other three (patients 5-7) were classified as having classic PMD. Myelination in the cerebral corticospinal tract, optic radiation, and corpus callosum was observed in three cases of classic PMD with PLP duplication. In patient 4, myelination extended to the internal capsule, corona radiata, and centrum semiovale over a 3-year period. No myelination was observed in three PMD cases with a PLP point mutation. T2 shortening in the deep gray matter was recognized in all patients with PMD. The presence of myelination in the cerebral corticospinal tract with diffuse white matter hypomyelination on MR images could be a marker for PMD with PLP duplication. It is suggested that progression of myelination may be present in connatal PMD with large PLP duplication.
  American Journal of Neuroradiology 20(10):1822-8. · 2.93 Impact Factor