Anatomy and physiology

豆狀核位於大腦半球深處而且內側與內囊有關，由內囊與尾核和丘腦分隔。豆狀核的外側與一層薄的白質稱為外囊(external capsule)，外囊與一層薄的灰質稱為帶狀核分隔。帶狀核再將外囊與腦島分隔。一個垂直的白質板將豆狀核分成較大而且顏色較深的外側部分稱為被殼(putamen)和內側顏色較淡的部分稱為蒼白球(globus pallidus)。蒼白球的顏色較淡是由於有髓鞘神經纖維的高度集中造成。在豆狀核的前端下方，被殼與尾核的頭部相連。

被殼的血液由後大腦動脈(MCA)的豆狀紋狀動脈(lenticulostriate a.)來提供。而這條動脈的外側分支，是最常發高血壓性腦出血(hypertensive hemorrhage)的地方，所以也被稱為The artery of cerebral hemorrhage。

Etiology

Hypertension 
Cigarette-smoker 
Alcohol ingestion 
Low serum cholesterol (<160mg/dL)

Incidence & mortality

The incidence rates are between 7 and 11cases per 100,000. Some Asian countries report several fold higher incidence rates of ICH (61/100,000).

Putaminal Hemorrhage in ICH: About 34% 
Mortality of putaminal hemorrhage: 37% 

Pathology 

The hemorrhage of putaminal, thalamic, and potine location occusr in the vascular distribution of the small, perforating intracerebral arteries, the lenticulostriate, thalamoperforating, and the basilar paramedian groups, respectively. Most of the ICHs originate from the rupture of small, deep arteries with diameters between 50 and 200μm. The same arteries are recognized to be those occluded in cases of lacunar infracts, a from of stroke correlated primarily with chronic hypertension and diabetes. Thus, it is apparent that these various groups of small arteries, located in well-defined anatomic areas, become the targets of chronic hypertension, and the result can be either occlusion or rupture, leading to lacunar infracts or ICH, respectively.

Vascular Rupture 

The actual mechanism leads to ICH is vascular rupture. HTN patients have higher incidence to have “military aneurysms” which means “blood collected outside the vessel wall” or “masses of blood”. The aneurysms are found mostly in the basal ganglia, internal capsule, and the thalamus, and less commonly in the centrum semiovale and cortical gray matter. Fisher concluded that HTN ICH most likely results rupture of one or two lipohyalinotic arteries, followed by sencondary arterial ruputures at the periphery of the enlarging hematoma in a cascade or avalanche fashion.

Pathologic Anatomy of Putaminal Hemorrhage  

The common putaminal variety originates at the posterior angle of this nucleus and spreads in a concentric fashion but generally extends more in the anteroposterior than the transverse diameter. The result is an ovoid mass of maximal anteroposterior diameter collected in the putamen and the structures located laterally to it, the external capsule and claustrum. The insular cortex is pushed medially or involved directly by the hematoma (Fig. 13-3). The origin of this form of ICH in the lateralposterior aspect of the putamen is bleeding from a laterally placed middle cerebral artery perforating branches are between 200 and 400μm wide at their entry to the brain, and they supply the putamen, internal capsule, and the head of the caudate nucleus. From its initial putaminal-claustral location, a sufficiently large hematoma may extend to other structures in the vicinities: medially into the internal capsule and lateral ventricle, superiorly into the corona radiate, and inferolaterally into the white matter of the temporal lobe.

These variations in the pattern of the extension result in clinical variants of the putaminal hemorrhage. The extension of the hemorrhage from its site of the origin can follow several patterns, the most common being dissection along the course of adjacent white matter fibers. The common medial extension of the hemotoma leads to communication with the laternal ventricle, through a process of slow leakage of blood rather than as direct communication between active bleeding site and ventricular system. Direct communication of the hematoma with the ventricular system, at times with associated hydrocephalus, is more likely to result from bleeding sites adjacent to the ventricular space, such as the thalamus and the head of the caudate nucleus. A putaminal hematoma that extends directly into the ventricle is usually large and thus is associated with high mortality.

Diagnosis

Symptoms & signs

1.          Flaccid hemiparesis 
2.          Hemisensory deficits 
3.          Homonymous hemianopia 
4.          Paralysis of conjugate gaze to the side of opposite the lesion / conjugate gaze to the side of the lesion 
5.          Mild to moderate impairment of consciousness.

另外，對於高階層功能(higher cortical functions)的影響為(常發生在沒有昏迷的病人當中)： 1.          Aphasia 
2.          Unilateral spatial neglect(USN) 

Hemiparesis, hemisensory deficits, conjugate gaze deviation的發生，有可能是因為血腫已經伸延(extension)到posterior limb of internal capsule，血腫可能壓迫或是影響到optic radiation。

Aphasia通常是因為左邊的被殼出血而造成的，原因可能是因為血腫的大小，血腫伸延(extension)的方向，波及到的白質(white matter)，以及波及到附近的神經路徑(fiber tracts)，在PET的研究中發現，在posterior middle temporal region的地方，glucose metabolism發生嚴重的不平均(left>right)。

有研究中發現，當把病人的失語症分成三種：non-aphasia, transient aphasia(only first 3 months), persistent aphasia，在persistent aphasia的病人當中，血腫伸延到temporal isthmus以及periventricular white-matter，但是non-aphasia的病人並沒有這樣情形發生。所以說，破壞到特定的白質部分才會引起失語症(aphasia)的產生。

Broca-type: hematomas extend anterior, involve much of deep frontal white-matter 
Wernicke-type: hemotomas extend posterior and temporal isthmus, temporal white-matter.

Global-type: hemotomas extend anterior and posterior and temporal isthmus

Conduction type: aracuate fasciculus fiber are interrupted, hemotomas extend laterally to external capsule and insula and just into temporal white-matter.

Non-dominant-hemisphere syndromes 
大約有82%的沒有昏迷的right putaminal hemorrhage都會有高階層的功能(higher cortical function)受到影響，如工作不能(apractognosia)，USN以及anosognosia(嗅覺缺失).

Non-dominant-hemisphere syndromes: 
1.          USN 
2.          Hemiasomatognosia(半邊軀體認識不能) 
3.          Anosognosia

Treatment

Prognosis 
病人的預後跟剛開始的神經症狀(initial neurologic severity)和血腫(volume of hematoma)有大小有關係。

Reference 
John C.M. Brust, Tohru Sawada, Seiji Kazui, Cerebral visual
    dysfunction. J.J.S. Barton and L.R. Caplan, Stroke Syndromes.
    Sencond edition. : Cambridge , 2001(Chap. 46, P590-598)

J.P.  Mohr, Dennis W. Choi, James C. Grotta, Bryce Weir, Philip A. Wolf.
    Stroke: pathophysiology, Diagnosis, and Management. Forth edition.
    Philadelphia : Churchill Livingstone, 2004(Chap 13, P327-376)

臨床神經解剖學 / Richard S. Snell 原著；劉亮延譯．--第一版，--台北巿新店巿：藝軒，2003【民92】(第10章, P315-3327)