Basal ganglionic hemorrhages

초록

Introduction The basal ganglia are the most common site of spontaneous hypertensive intracranial hemorrhage (ICH) [1–8]. In the pre-computed tomography (CT) era, Fisher's (1961) descriptions based on clinicopathological findings of very large basal ganglionic hemorrhages (BGH) were considered as the classical syndromes [9]. They included contralateral hemiplegia, hemisensory loss, hemianopia, ipsilateral conjugate gaze deviation, language dysfunction in dominant hemispheric lesions, and neglect in nondominant hemispheric lesions. However, with the advent of the CT scan, it was shown that hematomas with variable size could occur in the basal ganglia and their neighboring structures [10–12]. A variety of neurological features were reported according to the size and location of the BGHs [12–15]. In addition, in small BGHs, neurological deficits may mimic lacunar syndromes or may even be asymptomatic [16,17]. Hypertension is the most significant risk factor for developing BCHs (in more than 90% of cases), followed by chronic alcoholism, moyamoya disease, and cocaine use. In this chapter, we describe the classification of BGHs and the clinical features and prognosis of each type, except caudate nucleus hemorrhage, which is described in chapter 34. Anatomy of the basal ganglia Functional neuroanatomy of the basal ganglia The basal ganglia are composed mainly of the caudate nucleus, putamen, and globus pallidus, and are organized into five structurally and functionally distinct circuits. The circuits link the cerebral cortex, basal ganglia, and thalamus, with each circuit focused on a different portion of the frontal lobe (Figure 1 of Chapter 34) [18]. Two distinct loops pass through the basal ganglia: (i) a “motor” loop passing largely through the putamen, which receives inputs from the sensorimotor cortex, and the influences of which are ultimately transmitted to certain premotor areas, and (ii) an “association”(or “complex”) loop passing through the caudate nucleus, which receives input from the association areas, and the influences of which are ultimately returned to portions of the prefrontal cortex [18]. (See more detailed descriptions on the functional circuits in Chapter 34.) © Cambridge University Press 1995, 2001, 2012.