Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
ACV
Enfermedad que vascular que interrumpe las funciones del encfalo por alteraciones en la irrigacin de un territorio correlacionado con una arteria o vena.
ACV
Hemorrgicas
Hemorragias subaracnoidea Hemorragia intracerebral Traumtica:
Epidural Subdural
Vasoespasmo
Migraa
Otras causas
Amiloidosis Arteritis Migraosa Displasia fibromuscular Por radiacin Enfermedad de Moyamoma Alergia a contraste de angiografa
ACV
Otras causas
Sifiltico meningovascular Arteritis secundaria a meningitis tuberculosa Enfermedades mixtas del tejido conectivo (PAN, LES, Wegener, arteritis de la temporal, Takayasu, arteritis granulomatosa
ACV secuencia
Oclusin de vaso sanguneo Isquemia mas de 10 seg. Disminuye funcin corteza cerebral reversible Hipoxia sostenida por mas de 4 a 8 minutos= muerte neuronal. Disfucin cerebral Manifestaciones de acuerdo al rea afectada.
Compresin Carotdea
ARTERIA CEREBRAL MEDIA Y SU TERRITORIO reas de brodman 1,2,3, 4, 39,40, 44, 45, 5, 7, 41, 42, 22, ncleos basales
ACV isqumico de la cerebral media comprometera el territorio motor primario, lenguaje y sensitivo primario
ACV de ACM
Arterias lenticuloestriadas y de Heubner estan comprometidas (ramas de ACM), en el infarto estriatocapsular
Arteria cerebral anterior y su territorio, areas de brodman 8,9,10,11, 12, 4(paracentral), Arteria cerebral posterior 17, 18,19,28,34,36,37,29
ACV de C. Anterior
Perdida de motricidad y sensibilidad en MMII y genitales contralaterales (parcial o total) Desvia mirada y visin hacia el lado afectado. Reflejos aumentados que indican dao de primera motoneurona. Rigidez paratonica.- Del lado opuesto Afasia transcortical
ACV C. Anterior
syndrome de inatencin Abulia Amnesias Agitacin y psicosis Diskinesias y coreatetosis por isquemia de ncleo caudado y ganglios basales parte anterior. (aumenta con ejercicios prolongados)
nteromedial-inferior thalamic syndromes follow occlusion of the thalamoperforant branches. Here the most common effect is an extrapyramidal movement disorder (hemiballismus or hemichoreoathetosis or less often, asterixis). Deep sensory loss, hemiataxia, or tremor may be added in various combinations. Hemiballismus is usually a result of occlusion of a small branch to the subthalamic nucleus (of Luys) or its connections with the pallidum. Occlusion of the paramedian thalamic branches to the mediodorsal thalamic nuclei or to the dominant (left) mediodorsal nucleus is a recognized cause of an amnesic (Korsakoff) syndrome; this simulates infarction of the hippocampi from occlusion of the medial temporal branch of the posterior cerebral artery as noted below.
Hemianopsia
Disgrafias
Regiones irrigadas por arterias cerebrales posteriores, comunicantes posteriores y basilar (1) Arteria cerebral posterior (2) Arteria cerebelar superior (3) Arteria basilar (4) Arteria postero inferior (PICA) (5) vertebral artery (arteria cerebelosa antero inferior AICA, Arteria espinal anterior, Arterias espinales posteriores).
ACV hemorrgico
HTE
Cefalea HTA Nauseas Vomitos Fotofobia Edema de papila en fondo de ojo
lacunes are situated, in descending order of frequency, in the putamen and caudate nuclei, thalamus, basis pontis, internal capsule, and deep in the central hemispheral white matter. The cavities range from 3 to 15 mm in diameter, and whether they cause symptoms depends entirely on their location. Fisher, in several papers, has delineated the more frequent symptomatic forms of lacunar stroke: Pure motor hemiplegia Pure sensory stroke Clumsy handdysarthria Ipsilateral hemiparesisataxia A lacune in the territory of a lenticulostriate artery, i.e., in the internal capsule or adjacent corona radiata, usually causes a highly characteristic syndrome of pure motor hemiplegia involving the opposite face, arm, hand, leg, and foot in approximately equal measure. A lacune situated in the ventral pons causes an identical syndrome. In both cases, the lacunar syndrome is identified as much by its signature deficits as by those features that are absent; aphasia, apraxia, agnosia, and visual field defect. Symptoms may be abrupt in onset or evolve over several hours, but in some instances the neurologic deficit evolves stepwise and relatively slowly, over as long a period as 2 to 3 days.
Signs and symptoms 1. Medial medullary syndrome (occlusion of vertebral artery or branch of vertebral or lower basilar artery) a. On side of lesion (1) Paralysis with later hemiatrophy of the tongue b. On side opposite lesion (1) Paralysis of arm and leg sparing face (2) Impaired tactile and proprioceptive sense over half the body 2. Lateral medullary syndrome (occlusion of any of five vessels may be responsible vertebral, posterior inferior cerebellar, or superior, middle, or inferior lateral medullary arteries) a. On side of lesion (1) Pain, numbness, impaired sensation over half the face (2) Ataxia of limbs, falling to side of lesion (3) Vertigo, nausea, vomiting (4) Nystagmus, diplopia, oscillopsia (5) Horner syndrome (miosis, ptosis, decreased sweating)
Structures involved
Uncertainrestiform body, cerebellar hemisphere, olivocerebell fibers, spinocerebellar tract (?) Vestibular nuclei and connections Vestibular nuclei and connections Descending sympathetic tract
Spinothalamic tract
Corticobulbar and corticospinal tracts bilaterally Ocular motor nerves, apparatus for conjugate gaze, medial longitudinal fasciculus, vestibular apparatus
Visual cortex
Cerebellar peduncles and the cerebellar hemispheres
Tena factores de riesgo? Que territorios estn afectados?, tiene secuelas?, Quin es el personaje?, que le paso hace 1 ao y medio?