Youichi Ohnuki

Neuroimaging on delayed postanoxic encephalopathy with lesions localized in basal ganglia

A 59-year-old woman suffered from prolonged hypotension with myocardial infarction. Sixteen days after the episode, she showed bradykinesia, gait disturbance, and postural tremor. MRI revealed low signa intensities in the bilateral caudate nuclei and putamen on the T1-weighted image and high signal intensities on the T2-weighted image. PET with 18F-FDG revealed a severe decrease in glucose metabolism in bilateral basal ganglia. It is concluded that prolonged hypotension may induce localized delayed anoxic lesions in basal ganglia.

Chronological Changes in Cerebral Air Embolism That Occurred during Continuous Drainage of Infected Lung Bullae

We present a 43-year-old man with cerebral air embolism that occurred during continuous drainage of infected lung bullae. This complication is extremely rare, and may have been caused by the passage of air into the pulmonary venous circulation through a bronchovenous fistula and/or damaged pulmonary vessels. Air densities were demonstrated along the right frontal gyri on a CT performed 1 h after the onset of embolism, then moved to the deep cortex after 2.5 h. Three days later, a cortical infarct accompanied with extensive white matter edema in the right frontal lobe was confirmed by MRI. These CT and MRI findings may indicate the passage of intravascular air from the superficial to the deep cortex and subsequent cerebral infarction.

Mechanism of Reduction of Cortical Blood Flow in Striatocapsular Infarction: Studies Using [123I]Iomazenil SPECT

Single photon emission computed tomography (SPECT) using [123I]iomazenil (radioligand of central-type benzodiazepine receptors) was employed to examine two patients with striatocapsular infarction. Patient 1 was a 61-year-old female with motor aphasia and hemiplegia on the right side. Magnetic resonance imaging (MRI) showed a lesion in the anterior limb of internal capsule and putamen on the left side. SPECT using 99mTc-HMPAO revealed a reduction of cerebral blood flow (CBF) in the frontoparietal region on the left side, but the delayed images in SPECT using [123I]iomazenil showed only a mild decrease of accumulation in the frontal lobe. Patient 2 was a 55-year-old male with hemiplegia on the left side. MRI showed a lesion localized in the basal ganglia and posterior limb of the internal capsule on the right side. SPECT using 99mTc-HMPAO revealed a reduction of CBF in the frontoparietal region on the right side and in the cerebellar hemisphere on the left side, but the delayed images in SPECT using [123I]iomazenil showed little decrease of accumulation in parietal lobe. The discrepancy between CBF and receptor images suggested that cortical hypoperfusion on striatocapsular infarction might reflect hypometabolism due to disconnection of the neuronal network between subcortical structure and cortex.

Expanded Spectrum of Coagulopathy in the Etiology of Cerebral Infarction in Younger Adults in Japan

To clarify the role of coagulopathy in cerebral infarction (CI) in adults with onset before age 45, we performed comprehensive and repeated hemostatic analyses in 77 consecutive young adult patients w

[Hemichorea improved by carotid artery stenting in a 73-year-old man with hypoperfusion of the basal ganglia].

A 73-year-old man presented with continuous hemichoreic movement of right arm and leg and with dyskinesia in his tongue. Magnetic resonance image (MRI) showed no ischemic lesion within the basal ganglia, but magnetic resonance angiography (MRA) and carotid duplex ultrasonography showed the left internal carotid occlusion and 80% stenosis in the right common carotid artery. Tc-99m-ECD-SPECT showed hypoperfusion of the frontal lobe, temporal lobe, parietal lobe, basal ganglia and thalamus. A trial of haloperidol had no effect; therefore, the right carotid artery stenting was performed. Hypoperfusion in the left internal carotid artery area was improved by cross flow from the right side, and his hemichorea gradually improved. This result supports the notion that hypoperfusion-related hemichorea may occur, even in the absence of cerebral ischemia.