Ken-ichiro Hiramatsu

Specific Changes in Human Brain After Hypoglycemic Injury

BACKGROUND AND PURPOSE Very few reports are available on serial changes in the human brain after severe hypoglycemic injury. The aim of this study was to investigate sequential neuroradiological changes in brains of patients after hypoglycemic coma compared with those after cardiac arrest previously studied with the same methods. METHODS We repeatedly studied CT scans and MR images obtained at 1.5 T in four vegetative patients after profound hypoglycemia associated with diabetes mellitus. RESULTS In all patients, consecutive CT scans showed symmetrical, persistent low-density lesions with transient enhancement in the caudate and lenticular nuclei and transient enhancement in the cerebral cortex 7 to 14 days after onset. Serial MR images consistently revealed symmetrical lesions of persistent hyperintensity and hypointensity on T1- and T2-weighted images, respectively, in the caudate and lenticular nuclei, cerebral cortex, substantia nigra, and/or hippocampus from 8 days to 12 months after onset. CONCLUSIONS Repeated MR images revealed specific lesions in the bilateral basal ganglia, cerebral cortex, substantia nigra, and hippocampus, which suggests the particular vulnerability of these areas to hypoglycemia in the human brain. We speculate that the localized lesions represent tissue degeneration, including some combination of selective neuronal death, proliferation of astrocytic glial cells, paramagnetic substance deposition, and/or lipid accumulation. The absence of localized hemorrhages on MR images in hypoglycemic encephalopathy is in marked contrast to the presence of regional minor hemorrhages in postischemic-anoxic encephalopathy.

Specific changes in human brain following reperfusion after cardiac arrest.

Very few reports are available on serial changes in human brain after cardiac arrest. The pri-mary objective of this study is to investigate sequential neuro-radiological changes in patients remaining in a persistent vegetative state following resuscitation after cardiac arrest. Methods We repeatedly studied eight vegetative patients resuscitated from unexpected out-of-hospital cardiac arrest using computed tomographic (CT) scanning and high-field magnetic resonance (MR) imaging at 1.5 T. Results In seven of the eight patients, CT scans obtained between days 2 and 6 featured symmetrical low-density lesions in the bilateral caudate, lenticular, and/or thalamic nuclei. These ischemic lesions were persistently of low density on serial CT scans. In these seven patients, MR images demon-strated what were thought to be hemoglobin degradation products derived from minor hemorrhages localized in the bilateral basal ganglia, thalami, and/or substantia nigra. Dif-fuse brain edema in the acute stage and diffuse brain atrophy in the chronic stage were consistent neuroradiological findings. No abnormal enhanced lesions were demonstrated by CT scans. Conclusions The most characteristic findings on high-field MR images were symmetrical lesions in the bilateral basal ganglia, thalami, and/or substantia nigra with specific changes suggestive of minor hemorrhages that were not evident on CT scans. We speculate that these minor hemorrhages result from diapedesis of red blood cells in these regions during the reperfusion period through the endothelium disrupted by ischemia-reperfusion insult.

Hippocampal Damage in the Human Brain after Cardiac Arrest

Background and Purpose: Very few reports are available on changes in the human hippocampus after cardiac arrest. The objective of this study was to investigate if specific hippocampal volume losses can be demonstrated in the human brain following reperfusion after cardiac arrest. Methods: We assessed the volumes of the hippocampal formation (HF) and temporal lobe excluding HF (TL) as the contrast using magnetic resonance (MR)-imaging-based volumetry in 11 vegetative patients after cardiac arrest and in 22 healthy controls of similar age, sex and body size distribution. The measured volumes were normalized for differences in the head size among subjects by dividing by the total intracranial volume (TICV). The MR images of the 11 patients were obtained between days 8 and 21 after cardiac arrest. Results: The observed volumes of HFs and TLs of both patient and control groups were as follows: right HF volume (HFV): 2.67 ± 0.19 (mean ± SD, cm3) in patients versus 3.89 ± 0.44 in controls; left HFV: 2.72 ± 0.17 versus 3.74 ± 0.35; right TL volume (TLV): 73.37 ± 6.54 versus 80.08 ± 7.62, and left TLV: 72.45 ± 6.77 versus 78.59 ± 6.68. The normalized indices (HFV/TICV and TLV/TICV) were as follows: right HF: 0.0021 ± 0.0002 (mean ± SD) in patients versus 0.0031 ± 0.0001 in controls, p < 0.0001, left HF: 0.0022 ± 0.0002 versus 0.0030 ± 0.0001, p < 0.0001, right TL: 0.058 ± 0.002 versus 0.064 ± 0.004, p = 0.0007, and left TL: 0.058 ± 0.002 versus 0.062 ± 0.004, p = 0.0014. The HFV-TLV ratios (HFV/TICV divided by TLV/TICV) of both groups were: right HFV-TLV ratio: 0.037 ± 0.004 in patients versus 0.049 ± 0.004 in controls, p < 0.0001, left HFV-TLV ratio: 0.038 ± 0.004 versus 0.048 ± 0.004, p < 0.0001. Conclusions: The patient group had HFs that were 26.8–30.6% smaller than those of the control group, but in the patient group, the TLs slightly decreased in size by only 7.8–8.2% of the volume of those in the control group within 21 days after cardiac arrest. The volume reductions in the bilateral HFs of patients after cardiac arrest were significantly larger than those in the bilateral TLs. We speculate that this specific rapid hippocampal shrinkage reflects its greater vulnerability to global brain ischemia.

Delayed Ischemic Hyperintensity on T1-Weighted MRI in the Caudoputamen and Cerebral Cortex of Humans After Spectacular Shrinking Deficit

BACKGROUND AND PURPOSE Transient internal carotid artery (ICA)-middle cerebral artery (MCA) occlusion caused by cardiogenic embolus can lead to spectacular shrinking deficit (SSD): sudden hemispheric stroke syndrome followed by rapid improvement. The aim of this study was to investigate sequential neuroradiological changes in the brains of patients after SSD compared with those after brief cardiac arrest and hypoglycemia, which we previously studied with the same methods. METHODS We serially studied CT scans and MR images obtained at 1.5 T in 4 patients with SSD. All 4 patients suffered from transient neurological deficits due to cardiogenic embolus in ICA-MCA. The symptoms began to disappear from 25 to 50 minutes after onset. RESULTS Repeated CT scans demonstrated no abnormal findings in the affected cerebral hemisphere in 3 of the 4 patients and a small cortical infarct in the remaining 1. In each patient, repeated MRI between day 7 and month 23 after stroke showed basal ganglionic and cortical lesions. These lesions were hyperintense on T1-weighted and relatively hypointense on T2-weighted imaging. These ischemic lesions of hyperintensity on T1-weighted MRI subsided with time. CONCLUSIONS Transient ICA-MCA occlusion leading to SSD produces a specific ischemic change with delayed onset in the basal ganglia and cerebral cortex in humans on MRI but not CT scans. We speculate that the lesions represent incomplete ischemic injury, including selective neuronal death, proliferation of glial cells, paramagnetic substance deposition, and/or lipid accumulation. Unlike brief cardiac arrest or hypoglycemia, the localized lesions on MRI of patients after SSD seem to be incomplete and to differ from infarction or hemorrhage.

Use of Local Cerebral Blood Flow Monitoring to Predict Brain Damage after Disturbance to the Venous Circulation

A RAT MODEL of cortical vein occlusion by the photochemical thrombotic technique was used to evaluate whether monitoring the change in the local cerebral blood flow (LCBF) could predict brain damage after cortical vein occlusion. The cortical vein occlusion was attained by using the photochemical thrombotic technique, and the sequential LCBF was measured by using a laser Doppler flowmeter positioned over the middle frontal cortex between two adjacent dorsal veins for 120 minutes after the start of the irradiation to the cortical vein. Rats were assigned to one of three experimental groups. In Group A (n = 10), one dorsal cerebral vein was occluded ; in Group B (n = 10), two adjacent dorsal cerebral veins were occluded ; and in a sham-operated group (n = 5), the rats also underwent craniotomy and light exposure but received injections of saline rather than the rose bengal dye. After 24 hours, the rats were submitted to perfusion fixation and were examined histopathologically. After irradiation-induced cortical vein occlusion, a gradual and significant decrease of the LCBF was observed in both Group A (significantly different from the LCBF of the sham-operated group after 90 min, P 40% decrease at 120 minutes after the irradiation had severe brain damage. We conclude that continuous monitoring of the LCBF could be reliable and useful for predicting brain damage after cortical vein occlusion, and that the rat model of cortical vein occlusion by the photochemical thrombotic technique is useful for studying the pathophysiology of the venous circulation. (Neurosurgery 37 :280-286, 1995)

Changes in the basal ganglia and thalamus following reperfusion after complete cerebral ischaemia.

We report specific changes bilaterally in the basal ganglia and thalamus following reperfusion after complete cerebral ischaemia. A 69-year-old man, resuscitated after cardiac arrest, showed symmetrical lowdensity lesions in the head of the caudate nucleus and lentiform nucleus on CT. MRI revealed methaemoglobin derived from minor haemorrhage in the basal ganglia and thalamus, not evident on CT. We suggest that this haemorrhage results from diapedesis of red blood cells through the damaged capillary endothelium following reperfusion.

Profiles of an intravenously available endothelin A-receptor antagonist, S-0139, for preventing cerebral vasospasm in a canine two-hemorrhage model

We examined the prophylactic effect of a novel nonpeptide endothelin (ET) A-receptor selective antagonist, S-0139, using a canine two-hemorrhage model and an ET-1-induced cerebral vasospasm model. The agent markedly prevented cerebral vasospasm in the canine two-hemorrhage model when given intracisternally or intravenously by continuous daily dosing. An efficacious intravenous method was to apply a relatively high initial dose followed by daily sustaining administration at a much lower dose, which alone would have been ineffective. The need for sustaining dosing may imply daily successive attacks of ETs in the cerebral vessel compartment after the introduction of autologous blood into the subarachnoid space. A small amount of S-0139 was detected from the cerebrospinal fluid (CSF) with an apparent lag time after its disappearance from the plasma following intravenous dosing of 0.83 mg/kg/min for 12 min, however, cerebral vasoconstriction induced by ET-1 dosing from the adventitial side was clearly inhibited during such a lag period. Moreover, its movement into the CSF was greatly enhanced after the application of autologous blood to the animals. From these results, we conclude that ET-1 play a major role in producing delayed cerebral vasospasm in this canine two-hemorrhage model, and S-0139 effectively antagonizes the action of ET-1 even by intravenous treatment because it moves easily into the cerebral vessel compartment from plasma.

Expanding laminoplasty for cervical myelopathy-spinous process roofing technique

SummaryWe have carried out expanding laminoplasty using spinous process roofing technique for patients presenting with cervical myelopathy. The technique is a modified Kurokawas method. The result shows that laminoplasty with this technique provides better postoperative neck movement with a simpler surgical procedure. The clinical material consists of 54 cases with more than 3 years follow-up. Long-term investigation was performed focusing on the following three points, (1) bony fusion rates, (2) radiographic neck movement, (3) neurological improvement. The results indicate good postoperative bony fusion in all cases. Postoperative neck movement was also well preserved in the majority of cases.

Astrocytoma with widespread calcification along axonal fibres

SummaryWe describe a 44-year-old man found to have a diffusely calcified astrocytoma originating in the left frontoparietal region and extending along the axonal fibres into the opposite cerebral hemisphere and brain stem. Computed tomography and magnetic resonance imaging clearly demonstrated the spread of the tumour. The tumour was partially resected and histologically diagnosed as an astrocytoma. A correct preoperative diagnosis was difficult, because the lesion was very slow-growing and its widespread calcification mimicked congenital or inflammatory calcium deposits.

Microvascular changes associated with postischaemic hypoperfusion in rats

SummaryThe present study was undertaken to explore the cause of postischaemic hypoperfusion through morphological observations of the microstructure of brain cortex capillaries in rats with postischaemic hypoperfusion. Sixteen rats were used. The left middle cerebral artery of each animal was occluded for one hour (n = 8) or 2 hours (n = 8) and was followed by reperfusion for 2 hours. The regional cerebral blood flow (rCBF) of the ischaemia induced brain cortex was monitored continuously during the experiment and the microstructure of the brain cortex capillaries was then observed under electron microscope. Postischaemic hypoperfusion was observed in both ischaemia groups. The rCBF after 0.5 hours of reperfusion was significantly lower in the 2-hour ischaemia group than in the one-hour ischaemia group. The number of endothelial microvilli (MV) per capillary in the one-hour ischaemia group did not differ significantly from the control (the right cortex capillaries), whereas it was significantly higher in the 2-hour ischaemia group (p < 0.05). The ratio of the inner diameter to the outer diameter of capillaries decreased significantly in both ischaemia groups, and the ratio in the 2-hour ischaemia group was significantly lower than that in the one-hour ischaemia group (p < 0.05). Thus the present study statistically revealed that as postischaemic perfusion of the brains decreases, the number of MV increases, and endothelial cells swell more markedly. These microvascular changes seem to represent morphological factors associated with postischaemic hypoperfusion.