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This chapter presents a brief background on the rationale for how the cerebellum is engaged in non-motor functions. It discusses the relationship of the cerebellar motor syndrome to the higher order aspects of cerebellar dysfunction. The chapter analyzes the nature of the neuro-behavioral deficits and their relationship to cerebellar structure and vascular anatomy. It examines the clinical relevance of the cognitive and behavioral manifestations of cerebellar stroke in the diagnosis and management of patients with posterior circulation ischemia. In stroke neurology, the natural and appropriate tendency is to consider stroke syndromes as manifestations of occlusions of specific blood vessels. Bedside and office-based tests that the neurologist can administer to detect the cerebellar cognitive affective syndrome (CCAS) should focus on the domains known to be affected, namely, disorders of executive function, visuospatial cognition, language-based tests, and assessment of affect and other neuropsychiatric domains.
Acute, paroxysmal, recurrent, transient, permanent, progressive, or delayed movement disorders have been occasionally reported in the acute phase of stroke as well as after a delay of up to months or years (Kitanaka et al., 1995; Scott and Jankovic, 1996). Almost any type of hyperkinetic or hypokinetic movement disorder has been reported, most commonly as hemi- or focal dyskinesia. Only isolated case reports or very small series can be found in the literature, and few epidemiological studies (D'Olhaberriague et al., 1995; Ghika-Schmid et al., 1997) have been performed to estimate the prevalence of movement disorders in cerebrovascular disease. However, what is clear in all studies is that any kind of dyskinesia can be found with lesions at any level of the motor frontosubcortical circuits of Alexander et al., (1986), including the sensorimotor cortex, caudate, putamen, pallidum, subthalamic nuclei, thalamus, brainstem and interconnecting pathways (reviewed by Bhatia and Marsden, 1994).
Critchley (1929) introduced the concept of arteriosclerotic parkinsonism, characterized by clinical and pathological criteria, but his definition of this “disorder of the pallidal system” with “general rigidity of non-pyramidal type, weakness and slowness of movement” is somewhat different from what is accepted in the definition of the parkinsonian syndrome (requiring at least two items of bradykinesia, tremor, rigidity, and loss of balance or postural responses).
Parkinsonism of vascular origin is a controversial entity. Only 2% of patients with cerebral infarctsmay have a parkinsonian syndrome (Takeuchi et al., 1992). Acute hemiparkinsonism has been recently reported with infarcts in the area of the anterior cerebral artery (Kim, 2001a), large infarcts in the territory of the lenticulostriate arteries, sometimes in association with stereotyped movements (Kulisevsky et al., 1996), and exceptionally, in bilateral vascular lesions of the substantia nigra (Inoue et al., 1997). Subacute or delayed parkinsonism can occur after anoxia (postanoxic parkinsonism is also a well-known entity (Li et al., 2000) but it is rare to happen after a unilateral striatal infarct (Lazzarino et al., 1990).
In the 1960s and 1970s, the concept of vascular parkinsonism was discarded (reviewed by Parkes et al., 1974).
Acute, paroxysmal, recurrent, transient, permanent, or delayed movement disorders have been occasionally reported in the acute phase of stroke as well as after a delay up to months or years. Almost any type of hyperkinetic or hypokinetic movement disorder has been reported, most commonly as hemi- or focal dyskinesia. Only isolated case reports or very small series can be found in the literature, and few epidemiologic studies (D'Olhaberriague et al., 1995; Ghika-Schmid et al., 1997) have been performed in order to estimate the prevalence of movement disorders in cerebrovascular disease. However, what is clear in all studies, is the demonstration that any kind of dyskinesia can be found in lesions at any level of the motor frontosubcortical circuits of Alexander et al. (1986), including the sensorimotor cortex, caudate, putamen, pallidum, subthalamic nuclei, thalamus and brainstem and interconnecting pathways (for review, see Bhatia & Marsden, 1994).
Hypokinetic movement disorders
Parkinsonism associated with small vessel disease (‘vascular parkinsonism’)
Parkinsonism of vascular origin is a controversial entity. Only 2% of patients with cerebral infarcts may have a parkinsonian syndrome (De Reuck et al., 1980; Struck et al., 1990; Takeuchi et al. 1992). Hypertension is found in 22% of patients with parkinsonism (Marttila & Rinne, 1976, 1977). The association of ‘arteriosclerosis’ and parkinsonism has been studied, but does not seem to be significant (Eadie & Sutherland, 1964; Escourolle et al., 1970; Marttila & Rinne, 1976; Schneider et al., 1977; Kim et al., 1981; Horner et al., 1997; Homann & Ott, 1997).
Introduction: general concepts, anatomy, physiology, and neurochemistry
The basal ganglia have been associated with motor control since Wilson's Croonian lecture (1925), but Kleist (1922), and later others, extended their role to behavior, cognitive functions, emotions, motivation, reward, personality and character (for a summary, see Weiner and Lang, 1995). With their strategic location within the brain, and their rich and reciprocal connection with cortical sensorimotor areas, but also with limbic, paralimbic, midbrain, and diencephalic structures, the basal ganglia have all the rationale for processing the interface between internal personal drives (basic instincts, mood, motivations, needs) and the external world's stimuli, i.e., the modulation and motor expression of emotions, moods, needs, drives or motivation and cognition through corticospinal volitional axial and distal pathways (Kuypers, 1982), but also through emotional limbic motor-visceromotor pathways (Holstege, 1992).
The basal ganglia are included in retroactive loops on cortical activity and cannot any more be considered functional as separate anatomical entities. Therefore, a lesion at any level of this network can be followed by a common syndromic symptomatology. After a first attempt by Kleist (1922), Alexander et al. (1986) described five frontal-based ganglia-fhalamocortical segregated and parallel loops (there are probably more to discover), which have been designated as motor, oculomotor, dorsolateral prefrontal (DLPF), orbitofrontal (OF), and anterior cingulate (AC) fronto-subcortical circuits, which participate in the frontal management of primitive unmodulated drives and behaviors, that are ingrained in limbic, thalamic, and paralimbic structures. Each of these circuits has two pathways, one direct, projecting from the cortex to the caudate, external pallidum, internal pallidum/substantia nigra, and one indirect pathway, from external pallidum to the subthalamic nucleus and back to the internal pallidum, from where both circuits project together to the ventrolateral thalamic nucleus and back to their respective cortical areas.
The key role of the basal ganglia is their action as a filter, or gate processor on convergent motor, mood, and cognitive behavior (for a review, see Kimura and Graybiel, 1995). The overall activity of the basal ganglia is dichotomic, binary, organized within reciprocal zones of excitation and inhibition: either a release or activation, mediated by the direct pathways, promoting activity in recurrent, positive feedback loops, helped by dopamine, which also inhibits the indirect (inhibitory) pathway, or an inhibition or deficit, generated by the indirect inhibitor pathways, leading to the suppression of unwanted movements, thoughts, behaviors, or emotions.
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