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      Distonia virtual por infarto talâmico posterolateral ventral: relato de caso Translated title: Virtual dystonia due to a posteroventrolateral thalamic infarct: case report

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          Abstract

          O presente trabalho relata o caso de um diabético hipertenso acometido de uma forma fragmentária da síndrome de Dejerine-Roussy e "sensação de câimbra dolorosa" nos artelhos quando se deitava ou removia o pé do contato com o chão. A propriocepção estava acentuadamente comprometida nos artelhos que abrigavam a câimbra. Seu relato se adequava ao padrão das distonias fixas, não transcrita, todavia, como deformidade motora visível, razão pela qual designamos o fenômeno de "distonia virtual". A RNM mostrou imagem de infarto do núcleo lateral posterior do tálamo (VPL) e degeneração walleríana de projeções VPL-corticais. O SPECT, exclusão do tálamo e hipoperfusão do córtex parietal dorsal ipsilateral e dos núcleos da base bilateralmente. Sugerimos que, em decorrência da interrupção de aferentes propríoceptivos no tálamo, o córtex somestésico (S-I) originou atividade topograficamente ordenada, que emergiu sob a forma de distonia como representação mental subjetiva. Sugerimos que a distonia virtual represente o análogo somestésico das alucinoses unimodais, cujo exemplo mais conhecido é a síndrome de Bonnet.

          Translated abstract

          Behaviors, actions and movements may take place as purely mental events, as in the obsessions of obsessive-compulsive disorder, phantom limbs or sensory tics. In the present paper we report on the case of a 43-year-old diabetic hypertensive man who developed an incomplete form of the Dejerine-Roussy syndrome. Whenever he lay down or withdrew the leg from the ground, he experienced the illusion that the left intermediate toes painfully twisted and mounted each other. Conversely, as he stood up or firm pressure was artificially exerted against the sole, there was a dramatic relief from the "cramp" whose illusory character could he be certain of only by looking down at the foot. By passively moving his toes into the referred position we realized that the experienced deformity conformed to the pattern of a fixed dystonia not outwardly expressed through the motor system. There was severe proprioceptive loss in the same toes that harbored the cramp. MRI showed the appropriate lesion in the posteroventrolateral thalamus (VPL) and wallerian degeneration of thalamo-cortical projections. SPECT showed hypoperfusion of the overlying ipsilateral parietal cortex as well as of the basal nuclei bilaterally, besides the expected image of thalamic exclusion. We hypothesize that the infarct disconnected the somatic sensory cortex (S-I) from critical proprioceptive input with relative sparing of superficial sensibility. Lifting the foot deprived S-I of tonic inputs conveyed by undamaged contact-pressure pathways, a functional effect promptly reversed by placing the foot back against the ground. The case illustrates how a capricious deafferentation of S-I by a discrete VPL thalamic infarct might facilitate the emergence of autochthonous activity in the primary somesthetic cortex and give rise to a purely mental abnormal involuntary movement akin to the unimodal hallucinoses of which the syndrome of Bonnet is the best-known example. Virtual abnormal involuntary movements may be concealed more often than appreciated by complaints such as pains or cramps in patients with nervous system lesions.

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          Lateral Thalamic Infarcts

          A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.
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            NONHAEMORRHAGIC THALAMIC INFARCTION: CLINICAL, NEUROPSYCHOLOGICAL AND ELECTROPHYSIOLOGICAL FINDINGS IN FOUR ANATOMICAL GROUPS DEFINED BY COMPUTERIZED TOMOGRAPHY

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              Neuropsychological Assessment

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                Author and article information

                Journal
                anp
                Arquivos de Neuro-Psiquiatria
                Arq. Neuro-Psiquiatr.
                Academia Brasileira de Neurologia - ABNEURO (São Paulo, SP, Brazil )
                0004-282X
                1678-4227
                September 1996
                : 54
                : 3
                : 484-489
                Affiliations
                [01] orgnameUNI-RIO orgdiv1Hospital Universitário
                [02] orgnameUFRJ
                [03] orgnameHospital da Beneficiência Portuguesa
                Article
                S0004-282X1996000300020 S0004-282X(96)05400320
                10.1590/S0004-282X1996000300020
                3b91e089-720f-41e5-b9f6-21a693a9a78f

                This work is licensed under a Creative Commons Attribution 4.0 International License.

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                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 21, Pages: 6
                Product

                SciELO Brazil


                alucinose somestésica,distonia,alucinação,síndrome talâmica,thalamic syndrome,dystonia,somesthetic hallucinosis,hallucination

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