Neglect Syndrome in Hemisphere Stroke

The high incidence of cerebral stroke (CS) determinesthe great social importance of this problem [1–5]. More thanfive million people die every year from CS; in most countries,stroke is the second or third most common cause of death [6].CS has an important role as a cause of population disability –less than 20% of people who have had CS are able to returnto work and nearly 40% require nursing care [2, 5, 6].

The mechanisms of development of CS have now beenwell studied [7]. A role has been demonstrated for transfor-mation of the penumbra zone in neurorehabilitation process-es in hemisphere CS (HCS) [8, 9]. The pathological systemsconsisting of neuron ensembles in the tegmentum of thebrainstem and mediobasal structures can alter the functionalactivity of other neurons, leading to the development ofuncontrolled spike streams into the newly formed closedbrain system [10, 11]. More significant is the existence ofhyperactive neurons, with adverse influences on cerebralstructures and the ability to inhibit repair processes in thebrain. These pathological systems arising in HCS can induceclinical syndromes due to the involvement of structures farfrom the focal lesion, particularly neglect syndrome (NS)[12, 13]. The development of this syndrome involves mes-encephalic-diencephalic structures, the reticular formation,and other nonspecific formations which are damaged in theacute phase of HCS via cerebral edema and transtentorialdisplacement of the cerebral hemispheres, as well as circu-latory lesions [14, 15]. The process also involves the thala-mus, basal ganglia, corpus callosum, frontal lobe, and pari-etal and temporal lobes [16–18]. NS can be regarded as theconsequence of changes in the functional activity of braintissue by pathological systems [10, 19].

The aim of the present work was to study the mecha-nisms of formation of NS in acute stroke.

MATERIALS AND METHODSA total of 26 patients with NS were studied, of which

16 patients (61%) had experienced carotid ischemic CS and10 patients (39%) had had supratentorial hemorrhagic CS.Mean age was 50.6 ± 1.4 years.

Right-hemisphere CS was diagnosed in 71% of patientsand left-sided in 29%. CS developed on the background ofatherosclerosis of the cerebral arteries, arterial hypertension,diabetes mellitus, and their combinations. The severity andtype of motor impairments were studied using an originalscale for the integrated assessment of motor pathology(IOPM) and the unified clinical classification of motor syn-dromes (UKKDS) [20]. The type, location, and volume oflesions were determined using CT scans. The functional sta-tus of the brain was evaluated using EEG studies.

Results were analyzed statistically in SPSS 13.0.

RESULTS AND DISCUSSIONThe clinical picture in all 26 patients consisted of the

neurological syndromes of focal lesions of brain matter anddisorders due to diffuse damage on the background of exist-ing vascular risk factors. Focal neurological deficit consist-ed of hemiparesis of different severities with heterogeneousimpairments to muscle tone; a pathological posture devel-oped with a combination of flexion of the upper limbs anddrooping of the shoulder on the side of the paresis. Gait hadelements of spastic-paretic walking, with small steps andhypo- and bradykinesias. There was mild bilateral, lessoften unilateral static upper limbs tremor. The structure ofneurological disorders included psychopathological syn-drome with severe cognitive impairments, emotional-voli-

Neuroscience and Behavioral Physiology, Vol. 44, No. 3, March, 2014

Neglect Syndrome in Hemisphere Stroke

L. A. Shevchenko

0097-0549/14/4403-0320 ©2014 Springer Science+Business Media New York

320

Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 112, No. 12, Iss. II, Stroke,pp. 40–42, December, 2012.

Keywords: neglect syndrome, carotid stroke, treatment.

Zaporozhie State Medical University, Ukraine; e-mail: ludmilashev40@mail.ru.

tional disorders, and significant changes in baseline mood(see Table 1).

The clinical structure of the post-stroke motor deficitconsisted of varying degrees of paresis of the upper andlower limbs, with diverse combinations, variable types ofmuscular hypertonia, dissociation between the clinical signsof muscle weakness (paresis of 4–4.5 points) and the inabil-ity to perform or difficulty with fine differentiated move-ments of the fingers of the paralyzed hand. Studies of thestrength of the connection between individual clinical signsby correlation analysis supported the suggestion that therewas variability in individual symptoms, reflecting the clini-cal structure of post-stroke motor deficit. A close correla-tional relationship was demonstrated between criteria suchas muscle spasticity and less severe criteria – between thedegree of motor deficit and pyramidal symptoms, whichmay provide evidence for the role of the functional state ofthe cerebral structures and anterior horn formations con-trolled by the top-down reticulospinal systems of the brain informing the features of neurological deficit. Extrapyramidalimpairments were also frequent, in the form of oligo-, brady,and hypokinesia, and plastic muscular hypertonia, which insome patients were combined with hyperkinesia – statictremor of the limbs and, more rarely, the head.

Computerized tomography (CT) brain scans revealedfocal changes due to HCS, as well as changes in the area ofthe internal capsule, basal ganglia (most commonly theglobus pallidus) and the subcortical white matter of the tem-poral-parietal and, more rarely, the parietal-frontal lodes ofthe brain. Apart from these changes, all patients showedsigns evidencing the presence of encephalopathy – paraven-tricular leukoaraiosis and cortical atrophy. Comparison ofclinical and CT findings revealed an ambiguous relation-ship between the clinical structure of post-stroke neurolog-ical deficit and the morphological brain tissue defect. Therewas dissociation between the small size of the focal lesion(20–25 mm3) and the severity of the motor deficit and theminor therapeutic effects.

EEG studies demonstrated asymmetrical diffuse disor-ganization of brain bioelectrical activity, which consisted of

rhythms of intermediate and high amplitude (250 μW andmore) with a predominance of δ activity located in the cen-tral and temporal-frontal leads. α and β activity was minimal(less than 10% of total activity). Changes in the structure ofα activity were seen with the appearance of an α-like rhythmand polyphasic activity alternating with slow-wave, low-amplitude activity in the parietal-occipital leads. The β rhythmwas polyphasic and of low amplitude (less than 10 μW).

In addition, signs of hypersynchronization in patientswith NS were not seen; paradoxical reactions in functionaltests (activation reactions on photo- and phonostimulation)were also absent. Focal activity consisted of bilateral, morerarely unilateral, foci of slow-wave, high-amplitude activity(greater than 200 μW) in the temporal and temporal-parietalareas.

CONCLUSIONSThis study supported the polymorphism of motor

deficit in patients with HCS, who showed various extrapyra-midal defects affecting the clinical structure of the neuro-logical deficit [20, 21]. The development of NS after HCSwas due to the involvement of a variety of anatomical for-mations in the pathological process, including the thalamus,basal ganglia, corpus callosum, and rostral areas of thebrainstem [14, 16, 22].

There is potential for studies of the efficacy of usingmetabolic agents in the treatment of patients – particularlyGABAergic substances and agents limiting the effects ofexcitotoxicity, along with neurorehabilitation. Further stud-ies of the problem of NS and improvements in treatmentmay increase the efficacy of therapy and improve patients’quality of life.

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TABLE 1. Clinical Structure of Neurological Syndromes in Patients with HCS and NS (number of patients)

Clinical structure of neurological deficit Clinical structure of extrapyramidal system disorders

motor deficitsensory

syndromemotivational-volitional

statusakinesia

hypokinesia,bradykinesia

muscularplastic rigidity

hyperkinesia

contralateral ipsilateral bilateral

Hemiparesis 2.5–3 points4 (15.38%)

Hemianesthesia7 (27%)

Weakened9 (34%)

2 (8%) 24 (92%)grade 19 (34%)

11 (42%) 4 (15%) 7 (27%)

Hemiparesis 3–3.5 points15 (57.69%)

Hemianesthesia19 (73%)

Significantly weakened9 (34%)

grade 210 (38%)

Hemiparesis 3.5–4 points7 (26.92%)

Severely weakened8 (31%)

grade 37 (27%)

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