Takashi Kanda — Page 2

PubMed2003

[Multiple cerebral embolism caused by a patent foramen ovale and a uterine myoma].

Recently, patent foramen ovale(PFO) has been highlighted as an important risk factor of cerebral infarctions in young adults. We report a patient of multiple cerebral embolism associated with PFO and deep venous thrombosis caused by a uterine myoma. A 40-year-old woman suddenly suffered from right hemiparesis with motor aphasia. Brain angiography showed an occlusion of M2 portion of the left middle cerebral artery, but atherosclerotic changes were not seen. She developed left facial paresis 23 days later and admitted to our hospital. Brain MRI revealed multiple cerebral infarcts in the left insular cortex, the deep white matter of the right frontal lobe, and bilateral thalamus. Hypoxia with the perfusion defects of S1 and S2 sections of the right lung demonstrated by scintigraphy suggested pulmonary embolism. Transesophageal echocardiography showed a PFO with spontaneous left-to-right shunt and right-to-left shunt evoked by the Valsalva maneuver. Although venography could not detect thrombi, it revealed severe compression of the right external iliac vein by a uterine myoma. These findings suggested thrombi in the right external iliac vein were the embolic source when combined with elevated coagulation markers. An uterine myoma should be considered as an important risk factor for an embolic source in case of cerebral embolism with PFO.

Adult↗

PubMed2003

[Two distinct types of neuropathy associated with Sjögren's syndrome developed in one patient. The importance of the selection of an appropriate therapeutic regimen].

A 62-year-old woman was admitted to our hospital because of muscle weakness and sensory disturbance in extremities. She showed weakness, muscle atrophy and sensory abnormality in four limbs with patchy distribution, suggesting involvement of multiple peripheral nerve trunks. Serum titers of anti-SS-A, SS-B, and antinuclear antibody were elevated. Sural nerve biopsy showed recanalization and lymphocytic infiltration in the epineural small vessels, suggesting the presence of vasculitis. She was diagnosed as having vasculitic neuropathy complicated with Sjögren's syndrome. Methylprednisolone pulse therapy followed by oral prednisolone was started and these symptoms gradually improved in one month. At age 63, she felt dysesthesia in the right lower limb and this sensory abnormality spreaded to upper limbs. Two years later, she was admitted again due to clumsiness of hands and gait disturbance. Neurological examination showed decreased vibration and position sense of lower limbs and limb ataxia in addition to dysesthesia. Electrophysiological studies demonstrated significant decrease in amplitude of sensory nerve action potentials and delayed somatosensory evoked potentials after N13, indicating impairment of dorsal root ganglions. She was treated with intravenous immunoglobulin (400 mg/kg, total 15 g/day) for 5 days. One week later, sensory ataxia was improved. It has been known that Sjögren's syndrome is often complicate with various types of neuropathies including vasculitic neuropathy and sensory neuropathy. Our patient developed these two different types of neuropathies which were dramatically improved after two different therapeutic regimens; indicating the importance to select a suitable treatment regimen in accordance with the mechanism of neuropathy associated with Sjögren's syndrome.

Adrenal Cortex Hormones↗