・パーキンソン病患者の研究（Ketcham et al., 2003） 尾状核は空間情報の記憶から動作への変換に関与
・パーキンソン病患者 疾患の初期段階のワーキングメモリー障害: 非空間的＜空間的
Alexander et al.(1986)の「皮質-線条体回路」
（Emre Kumral, MD, PhD; Dilek Evyapan, MD, PhD Kaan Balkir, MD. Acute Caudate Vascular Lesions. Stroke. 1999;30:100-108
Background and Purpose—We sought to evaluate demographic features, risk factors, clinical profiles, and behavioral abnormalities in patients with caudate lesion, either with infarct or with hemorrhage involving the caudate nucleus.
Methods—We studied all patients with acute caudate stroke confirmed by CT or MRI who were admitted to our stroke unit over a 5-year period. A database containing risk factors, clinical features, type and mechanism of stroke, and caudate vascular territories was analyzed.
Results—Thirty-one patients had acute caudate stroke (24 men and 7 women; mean age, 62.3 years). Caudate infarct was present in 25 patients and caudate hemorrhage in 6. The main risk factors for caudate infarct were hypertension (64%), hypercholesterolemia (32%), diabetes mellitus (28%), and previous myocardial infarct (20%). Hypertension was present in 4 patients (67%) with caudate hemorrhage, and arteriovenous malformation was present in 1 patient (17%). Small-artery disease was diagnosed in 14 patients (59%), cardiac embolism in 5 patients (20%), and large-artery disease in 2 patients (8%), and 2 patients (8%) had mixed etiology. The most frequent neurological abnormalities were abulia and psychic akinesia (48%), frontal system abnormalities (26%), speech deficits in patients with left-sided lesions (23%), and neglect syndromes in those with right-sided lesions (10%). Fifteen patients with caudate infarct (60%) and 3 patients with hemorrhage (50%) were able to return to normal daily life. Patients with infarct in the territory of the lateral lenticulostriate arteries extending to neighboring structures showed more frequent motor and neuropsychological deficits than those with infarct in the territory of the anterior lenticulostriate arteries.
Conclusions—The clinical presentation of patients with caudate hemorrhage mimicked subarachnoid hemorrhage with or without motor and neuropsychological signs. Caudate vascular lesions with concomitant neighboring structure involvement represent a specific stroke syndrome, usually caused by small-artery disease and in one fifth of the patients caused by cardiac embolism. The behavioral abnormalities were mostly due to medial, lateral, and ventral caudate subnuclei damage and coexisting lesion of the anterior limb of the internal capsule.
Long-term Cognitive Impairment Associated With Caudate Stroke
Hirokazu Bokura, MD; Robert G. Robinson, MD. Stroke. 1997;28:970-975
Background and Purpose Neuropsychiatric findings were examined in 91 patients with acute focal subcortical lesions to determine whether cognitive outcome would differ depending on whether the head of the caudate or other subcortical structures were injured.
Patients were evaluated using the Mini-Mental State Examination (MMSE), Hamilton Rating Scale for Depression, and modified Present State Examination. Patients were reexamined at short-term (3 to 6 months) or long-term (1 to 2 years) follow-up.
There were no significant intergroup differences in the MMSE scores at the initial evaluation or at short-term follow-up. At long-term follow-up, however, patients with either right or left caudate lesions had significantly lower MMSE scores than patients with other subcortical lesions.
Conclusions A significant number of patients with caudate infarction deteriorate in their intellectual function between 1 and 2 years after stroke. This phenomenon could be mediated through disruption of cortical projections to the caudate.
てんかん重積後の所見に類似していたが、cortical laminar necrosisが見られたかどうかが、鑑別になるのではないかのコメントがあった。
Kristina Szabo, MD; Alex Förster, MD; Theodor Jäger, PsyD; Rolf Kern, MD; Martin Griebe, MD; Michael G. Hennerici, MD Achim Gass, MD. Hippocampal Lesion Patterns in Acute Posterior Cerebral Artery Stroke. Clinical and MRI Findings Stroke. 2009; 40: 2042-2045
Background and Purpose— Reports of ischemic stroke affecting the hippocampus are rare. In this study we used diffusion-weighted MRI (DWI) to characterize patients with posterior circulation stroke involving the hippocampus.
Methods— Fifty-seven consecutive acute stroke patients with hippocampal infarct (HI) on DWI were analyzed with regard to clinical features and ischemic lesion patterns. The last 20 of these underwent additional neuropsychological testing of short-term, working, and episodic long-term memory.
Results— We found unilateral HI in 54 and bilateral HI in 3 patients. Visual analysis identified 4 patterns of DWI lesion affecting (1) the complete hippocampus (15/60), (2) the lateral (19/60) or (3) dorsal (22/60) parts of the hippocampal body and tail, and (4) circumscribed lesions in the lateral hippocampus (4/60), corresponding well to hippocampal vascular anatomy. In all cases DWI showed further ischemic lesions in the posterior circulation. Symptoms from lesions outside the hippocampus were the common leading clinical signs. Whereas mnestic deficits were prominent in only 11/57 patients, neuropsychological examination in 20 patients showed deficits of verbal episodic long-term memory in left and of nonverbal episodic long-term memory in right HI.
Conclusion— Several phenotypic lesion patterns can be distinguished in HI that usually occur as part of multifocal PCA ischemia. A careful neuropsychological examination is necessary to detect resulting memory deficits.
Figure 1. We identified 4 different patterns of acute ischemic lesions of the hippocampus corresponding to the vascular anatomy and affecting either the complete hippocampus (A), the lateral (B) or dorsal (C) parts of the hippocampal body and tail, and small circumscribed lesions in the lateral hippocampus (D). The lesion patterns are presented as schematic drawings (1–4) and as DWI hyperintense acute ischemic lesions (A–D). The possible vessels involved are the proximal posterior cerebral artery (PCA; A), the longitudinal terminal segments of the hippocampal arteries (B), and the middle or posterior hippocampal artery (C). The small lesions might be explained by distal emboli (D). Note that in right image the anterior hippocampal artery is not shown; it is partly hidden by the PCA and the basal vein and disappears into the uncal sulcus.
Szabo K, Poepel A, Pohlmann-Eden B, Hirsch J, Back T, Sedlaczek O, Hennerici M, Gass A. Diffusion-weighted and perfusion MRI demonstrates parenchymal changes in complex partial status epilepticus. Brain. 2005; 128: 1369–1376.
Diffusion-weighted MRI (DWI) and perfusion MRI (PI) have been mainly applied in acute stroke, but may provide information in the peri-ictal phase in epilepsy patients. Both transient reductions of brain water diffusion, namely a low apparent diffusion coefficient (ADC), and signs of hyperperfusion have been reported in experimental and human epilepsy case studies. We studied 10 patients with complex partial status epilepticus (CPSE) with serial MRI including DWI and PI. All patients showed regional hyperintensity on DWI, and a reduction of the ADC in (i) the hippocampal formation and the pulvinar region of the thalamus (six out of 10 patients), (ii) the pulvinar and cortical regions (two out of 10), (iii) the hippocampal formation only (one out of 10), and (iv) the hippocampal formation, the pulvinar and the cortex (one out of 10). In all patients a close spatial correlation of focal hyperperfusion with areas of ADC/DWI change was present. In two patients hyperperfusion was confirmed in additional SPECT (single photon emission computed tomography) studies. All patients received follow-up MRI examinations showing partial or complete resolution of diffusion and perfusion abnormalities depending on the length of the follow-up interval. The clinical course, EEG and SPECT results all indicate that MRI detected changes related to prolonged epileptic activity. Combined PI and DWI can visualize haemodynamic and tissue changes after CPSE in the hippocampus, thalamus and affected cortical regions.
Diffusion-weighted MRI demonstrating involvement of the hippocampus in patients 3, 4, 6, 7 and 9. High-intensity signal abnormality is noted in the right (A) and left (B–E; arrows) hippocampus. Hyperintense susceptibility artefacts can occasionally be seen in the area of the temporal bone.
Cortical laminar necrosis related to prolonged focal status epilepticus.
Donaire A, Carreno M, Gómez B, Fossas P, Bargalló N, Agudo R, Falip M, Setoaín X, Boget T, Raspall T, Obach V, Rumiá J. J Neurol Neurosurg Psychiatry. 2006 Jan;77(1):104-6.
AbstractCortical laminar necrosis (CLN) is radiologically defined as high intensity cortical lesions on T1 weighted MRI images following a gyral distribution. Histopathologically, CLN is characterised by pannecrosis of the cortex involving neurones, glial cells, and blood vessels. It has been reported to be associated with hypoxia, metabolic disturbances, drugs, and infections. We present two patients who developed CLN and permanent neurological deficits after prolonged and repeated focal status epilepticus. The possible mechanisms leading to CLN in these patients are discussed, together with the implications of prompt and aggressive treatment in similar cases.
Figure 1(A) Ictal 99mHMPAO SPECT demonstrating right temporo‐parieto‐occipital hyperperfusion. (B1–2) Axial T2 weighted images showing cortical increased signal intensity of the right temporo‐parieto‐occipital regions compatible with transient radiological changes associated with SE. B1 corresponds to the first SE. Notice the extensive cortical and white matter oedema associated with the brain abscess compared to the exclusively cortical oedema related to radiological changes associated with SE. The patient recovered after the first SE without significant neurological deficits. B2 corresponds to the second SE. At this time the oedema was mostly cortical and there were no signs of acute infection in the temporal region. (B3–4) Follow‐up MRI, 3 weeks after the second SE. Axial and sagittal T1 weighted images show a high intensity cortical laminar lesion following a gyral distribution associated with volume loss in the right posterior temporal, parietal, and occipital regions, indicative of CLN. Notice also a hyperintense lesion on T1 weighted images located at the posterolateral portion of the ipilateral thalamus (C2). (C1–2). Axial T1/T2 weighted images showing cortical increased signal intensity on T2 weighted images (C1) of the left parietal region and decreased signal intensity in the exact same location in T1 weighted images (C2) during the first SE. Notice the absence of hyperintense cortical lesions in the posterior quadrant during the first SE in C2. (C3–4) Follow up MRI, 1 week after the second SE. Axial and sagittal T1 weighted images show a high intensity cortical lesion following a gyral pattern associated with volume loss in the left posterior temporal, parietal, and occipital regions.
Ann Neurol. 1996; 39(6):779-88.
The syndrome of posterior choroidal artery territory infarction.
Neau JP, Bogousslavsky J.
Posterior choroidal artery (PChA) territory infarcts remain the least well-known type of thalamic infarcts. Our study of 10 personal cases, selected from 2,925 stroke patients admitted consecutively to a community-based primary care center, and 10 published cases of unilateral PChA territory infarct suggests that they can often be differentiated clinically from other thalamic infarcts. Patients with PChA territory infarct associated with superficial posterior cerebral artery territory infarct or with another infarct were excluded. Damage was characteristically limited to the lateral geniculate body, pulvinar, posterior thalamus, hippocampus, and parahippocampal gyros, without involvement of the upper midbrain and the anterior nucleus of thalamus. In lateral PChA territory infarct, the most common clinical manifestations included homonymous quadrantanopsia, with or without hemisensory loss and neuropsychological dysfunction (transcortical aphasia, memory disturbances). A homonymous horizontal sectoranopsia is exceptional but particularly suggestive of the involvement of the lateral geniculate body in this territory. Media] PChA territory infarct was less frequent. Its neurologic picture was dominated by eye movement disorders not particularly suggestive of thalamic involvement. Late disability was usually absent or slight, being related to pain and delayed abnormal movements. The most common stroke etiology was presumed small-vessel occlusive disease.