Dihné Marcel, Grommes Christian, Lutzenburg Michael, Witte Otto W, Block Frank
Department of Neurology, Rheinisch Westfälische Technische Hochschule-Aachen, Aachen, Germany.
Stroke. 2002 Dec;33(12):3006-11. doi: 10.1161/01.str.0000039406.64644.cb.
After focal cerebral ischemia, depending on its localization and extent, secondary neuronal damage may occur that is remote from the initial lesion. In this study differences in secondary damage of the ventroposterior thalamic nucleus (VPN) and the reticular thalamic nucleus (RTN) were investigated with the use of different ischemia models.
Transient middle cerebral artery occlusion (MCAO) leads to cortical infarction, including parts of the basal ganglia such as the globus pallidus, and to widespread edema. Photothrombotic ischemia generates pure cortical infarcts sparing the basal ganglia and with only minor edema. Neuronal degeneration was quantified within the ipsilateral RTN and VPN 14 days after ischemia. Glial reactions were studied with the use of immunohistochemistry.
MCAO resulted in delayed neuronal cell loss of the ipsilateral VPN and RTN. Glial activation occurred in both nuclei beginning after 24 hours. Photothrombotic ischemia resulted in delayed neuronal cell loss only within the VPN. Even 2 weeks after photothrombotic ischemia, glial activation could only be seen within the VPN.
Pure cortical infarcts after photothrombotic ischemia, without major edema and without effects on the globus pallidus of the basal ganglia, only lead to secondary VPN damage that is possibly due to retrograde degeneration. MCAO, which results in infarction of cortex and globus pallidus and which causes widespread edema, leads to secondary damage in the VPN and RTN. Thus, additional RTN damage may be due to loss of protective GABAergic input from the globus pallidus to the RTN or due to the extensive edema. Retrograde degeneration is not possible because the RTN, in contrast to the VPN, has no efferents to the cortex.
局灶性脑缺血后，根据其定位和范围，可能会在远离初始病变的部位发生继发性神经元损伤。在本研究中，使用不同的缺血模型研究了丘脑腹后核（VPN）和丘脑网状核（RTN）继发性损伤的差异。
短暂性大脑中动脉闭塞（MCAO）会导致皮质梗死，包括基底神经节的部分区域，如苍白球，并导致广泛水肿。光血栓性缺血会产生单纯的皮质梗死，不累及基底神经节，且仅有轻微水肿。在缺血14天后，对同侧RTN和VPN内的神经元变性进行定量分析。使用免疫组织化学研究胶质细胞反应。
MCAO导致同侧VPN和RTN的神经元细胞延迟性丢失。胶质细胞激活在24小时后开始在两个核中出现。光血栓性缺血仅导致VPN内的神经元细胞延迟性丢失。即使在光血栓性缺血2周后，胶质细胞激活也仅在VPN内可见。
光血栓性缺血后产生的单纯皮质梗死，无严重水肿且对基底神经节的苍白球无影响，仅导致继发性VPN损伤，这可能是由于逆行性变性所致。MCAO导致皮质和苍白球梗死，并引起广泛水肿，导致VPN和RTN的继发性损伤。因此，额外的RTN损伤可能是由于从苍白球到RTN的保护性GABA能输入丧失或由于广泛水肿所致。由于与VPN不同，RTN没有传出纤维至皮质，所以不可能发生逆行性变性。
