Antinuclear antibody, is it a risk factor for cerebral ischemia? Magnetic resonance image analysis, a preliminary study.

Magnetic resonance images (MRI) of 103 patients were examined to reveal whether positive antinuclear antibody is a risk factor for cerebral ischemia. The most common MRI formation was the presence of small high-intensity spots. The prevalence of hypertension and diabetes mellitus was significantly low. Although seven cases had no medical risk factors; they showed an abnormal MRI reading. Eleven cases exhibited signs of cerebral stroke. Positive antinuclear antibody cases are suggested to be part of the antiphospholipid antibody syndrome. Various types of cerebral arterial occlusion may occur, showing lacuna, atheroma generation, and a recurrent major vessel occlusion.

Bilateral chronic subdural hematoma cases showing rapid and progressive aggravation.

BACKGROUND: We have analyzed the records of our own hospitalized cases of bilateral chronic subdural hematoma (cSDH) to reveal the prognosis. METHODS: Ninety-eight cases of cSDH were operated at our hospital over a 6-year period, in which 14 cases were classified as being bilateral. Among these 14 cases, 6 cases showed a rapid and aggressive clinical course. Therefore, complicated risk factors, the initial data on coagulofibrinolytic examination, magnetic resonance imaging appearance, and prognosis were analyzed. RESULTS: Of the 6 cases, 5 showed a rapid aggravation as they awaited surgery. The period of the aggravation since the initial diagnosis harboring cSDH was 19 to 54 hours. One case was at first neurologically free from any disturbance but 17 hours later experienced a generalized seizure. All 6 cases experienced consciousness disturbance. In addition, 3 of them manifested oculomotor palsy. Two cases showed an abnormality of coagulofibrinolytic activity. No significant risk factors were revealed. In 4 cases, T(2)-weighted images (T2WIs) revealed the hematoma of a mixed high and low intensity, indicating that the hematoma consisted of both liquid and solid parts of a freshly formed blood clot. In 2 cases, the hematoma showed a low intensity in T(1)-weighted image (T1WI), indicating a recent bleeding of a significant amount. CONCLUSION: The bilateral cases of cSDH should be treated as early as possible with simultaneous decompression of bilateral hematoma pressure, even if the patient shows minimal neurologic deficits. Mixed high and low intensity in T2WI or low intensity in T1WI is the most predictable factor to show rapid aggravation.

Incomplete oculomotor nerve palsy caused by an unruptured internal carotid-anterior choroidal artery aneurysm--case report--.

A 59-year-old woman visited our institute with the chief complaint of dizziness which persisted whenever she tried to focus on objects. She had not experienced apparent double vision and had no history of intracranial bleeding. Neurological examination revealed no abnormality except for exotropia at the mid-position and at upper gaze. Cerebral angiography revealed that the intracranial portion of the left internal carotid artery ran more horizontally and also identified an unruptured left internal carotid-anterior choroidal artery (IC-AChA) aneurysm of 3.0 mm diameter. The aneurysm at the origin of the AChA was confirmed during surgery. The proximal lateral wall of the aneurysm was in contact with the oculomotor nerve. This contact was released after complete obliteration of the aneurysm. The exotropia resolved 3 months later. Oculomotor nerve palsy usually indicates the presence of internal carotid-posterior communicating artery (IC-PcomA) aneurysm. Since sacrifice of the AChA will result in severe neurological deficits, accurate neuroimaging information is needed prior to the operation. Conventional angiography and/or three-dimensional computed tomography angiography should be performed to ascertain whether the aneurysm is an IC-PcomA or IC-AChA aneurysm, even if some neurosurgeons insist that conventional angiography is not always needed before surgery for an unruptured aneurysm.

[Two cases of transient global amnesia (TGA) immediately after coronary angiography: pathogenesis of the primary TGA].

Two cases of transient global amnesia (TGA) following coronary angiography are reported. Nonionic contrast media was used and injected at room temperature. Both cases showed sudden amnesia about 15 minutes after the left ventriculography. A clinical feature was typical to TGA, showing repeated questions with retrograde and antegrade memory disturbance without any other neurological abnormality. Diffusion-weighted images (DWI) of magnetic resonance imaging revealed no fresh lesion in both cases. The patients recovered from TGA attack within 24 hours. Some cases have been reported which display a manifested TGA following cerebral or coronary angiography. In these situations, embolism, the effect by the contrast media was suspected as the cause of TGA. Since most TGA cases in a classical meaning (primary TGA) showed no abnormality in both DWI and T2-weighted image (T2WI), the cerebral ischemia was not really considered to be the cause of the condition. Therefore, the pathogenesis of the TGA is suggested to be much more functional rather than anatomically abnormal. The pathogenesis of the primary TGA was thought to be some kind of hypersensitivity to the external stress or the stress reaction of the hippocampal cell. This stress may lead to cellular depolarization and the following repolarization (spreading depression), which showed transient abnormality in DWI and not a permanent abnormality in T2WI.

[A case of solitary and unilateral trochlear nerve palsy due to a blunt head impact].

A case of solitary and unilateral trochlear nerve palsy following a minor, blunt head impact is reported. A 72-year-old man fell down backwards from the top of a staircase having 13 steps and hit his right parietal head and shoulder. Routine neurological examination revealed no remarkable findings, however, the subject complained of double vision when he focused downwards. The computed tomography four hours after the initial impact showed a localized small high-density lesion on the left quadrigminal cistern. The magnetic resonance imaging also indicated subarachnoid bleeding expressed by the low-intensity area in T2 weighted images in the same place. There was no evidence of any contusion within the midbrain. Hess chart test clearly showed solitary left superior oblique muscle palsy. The manner of the injury was thought to be quite typical, since he had hit his right parietal area up-side-down when falling, that is, the accelerated force acted as an impact against the firm floor. This impact caused the midbrain concussion against the cerebellar tentorial notch resulting in a localized subarachnoid hemorrhage which caused the unilateral trochlear nerve palsy.