Localizando lesões

Question 1

Quais as sindromes de lobo frontal?

Answer 1

Frontal lobe functions: Mvmt: Mediated by 1° and supplementary motor areas; voluntary mvmt of eyes to opposite side: mediated by frontal eye fi elds; attention, planning, judgment, insight, abstract thinking; Lang: See below. Lesions involving the frontal lobe & clinical manifestations: Orbitofrontal synd: Disinhibition, impulsive behav; Frontal convexity synd: Apathetic, angry/aggressive behav. There may be assoc disturbances in mvmt. Medial frontal synd: Mutism, gait disturbances, & bladder incont.; Massive frontal lobe lesion: Akinetic, apathetic, & abulic state; Broca area: Inf frontal region in areas 44 & 45; resultant expressive aphasia characterized by nonfl uent speech w/ rel intact comprehension & impaired repetition, reading, & writing.

Question 2

Quais as sindromes de lobo parieral?

Answer 2

Parietal lobe functions: Sensation: Somatosens area in postcentral gyrus. Attention: An inf parietal lesion, typ nondominant → contralat hemispatial neglect, anosagnosia. Lesions involving the parietal lobe & clinical manifestations: Gerstmann synd: Lesion in dominant, inf parietal lobe → acalculia, alexia, fi nger agnosia, L-R confusion; Lesion of dominant angular gyrus: Alexia w/ agraphia; Balint synd: Bilat parieto-occipital lesions; often due to watershed infarcts between PCA & MCA territories. Sx incl optic ataxia, ocular apraxia, visual inattention, simultagnosia.

Question 3

Quais as sindromes de lobo temporal?

Answer 3

Temporal lobe functions: Recognition of stimuli. Hearing: Mediated by 1° auditory areas in transv temporal gyrus & 2° auditory areas in sup temporal gyrus; Memory: Med by hippocampus; Lang: See below. Lesions involving the temporal lobe & clinical manifestations: Prosopagnosia: Bilat or nondominant occipital temporal lesion → inability to identify or recognize faces. Kluver-Bucy synd: Bilat lesions of the medial temporal lobes or amygdala → hyperorality, hypersexuality, changes in emotional behav. Wernicke aphasia: Receptive lang disturbance w/ nonsensical fl uent speech w/ poor comprehension & repetition.

Question 4

Quais as sindromes de lobo occipital?

Answer 4

Occipital lobe functions: Vision (calcarine cortex): Lesions may cause blindness, vision loss, or visual agnosia. Lesions involving the occipital lobe & clinical manifestations: Anton synd: Bilat parieto-occipital lesions → unaware of blindness. Preserved pupillary light reaction. Palinopsia: Persistence of visual image for several minutes despite gazing at another scene. Often 2° to occipitotemporal dz or during recovery from cortical blindness. Alexia w/o agraphia: Dom occipital lobe & splenium of corpus callosum. Often accom by a R homonymous hemianopia & color naming defi cits.

Question 5

Quais lesões tem poder de lateralização hemisferica?

Answer 5

Lateralization of cerebral hemispheres: Right hemisphere: Spatial & constructional skills, nonvisuospatial perception, emotional tone of speech. Left hemisphere: Lang, analytic & mathematic skills, reasoning. Major white matter tracts connecting hemispheres: Corpus callosum, anterior commissure

Question 6

Quais são as sindromes das lesões das vias visuais?

Answer 6

Optic nerve: Ipsi monocular visual fi eld defects. Optic chiasm: Bitemporal hemianopia. Anterior chiasm synd: Ipsi monocular visual loss + contralat sup temporal defect (junctional scotoma). Due to compression of ipsi optic nerve & contralat inferonasal fi bers called Wilbrand knee, although the presence of this is controversial. Body of the chiasm synd: Bitemp visual fi eld defects (w/ or w/o splitting of macula). Posterior chiasm synd: Bitemp scotomas w/ intact periph fi elds. Optic tract: Contralat homonymous hemianopia. Optic radiations, inf division or meyer loop: Travels through temporal lobe. Contralat sup quadrantanopia. Optic radiations, sup division: Travels through the parietal lobe. Contralat inf quadrantanopia. Occipital lobe: Contralat homonymous hemianopia w/ macular sparing. Pupillary light refl ex: When light is shined in one eye, pupil constricts in ipsi & contralat eye (direct & consensual response, respectively); mediated by cranial nerves (CN) II & III. Pathway: Retina → optic nerve → optic chiasm → optic tract → pretectum → Edinger-Westphal nucleus → pregang parasympathetic fi bers in CN III → ciliary ganglion → pupillary constrictor muscles.

Question 7

Quais são os ganglios da base?

Answer 7

Components: Caudate, putamen, external & internal globus pallidus, subthalamic nucleus, substantia nigra pars compacta (SNPc) & pars reticulata. Striatum = caudate + putamen, lentiform nucleus = putamen + globus pallidus.

Question 8

Como funciona a substancia negra em relação aos nucleos da base?

Answer 8

Infl uence of the SNPc: Modulate activity of caudate & putamen (striatum). Two types of dopaminergic receptors in striatum: D1 & D2. D1: Excitatory to direct pathway. D2: Inhibitory to indirect pathway. Net effect of D1 & D2 activity is excitatory (or to decrease inhibitory infl uence of basal ganglia). In Parkinson’s dz, there is loss of dopaminergic neurons of SNPc.

Question 9

Quais as sindromes das lesões de NDB?

Answer 9

Lesions involving the basal ganglia & clinical manifestations: Subthalamic nucleus: Contralat hemiballismus. Caudate nucleus: Contralat choreoathetosis.
Globus pallidus: Contralat hemidystonia, hemiparkinsonism, tremor. Substantia nigra: Parkinsonism. Unilat basal ganglia: Falling to contralat side & slow mvmts

Question 10

Quais as porções do talamo?

Answer 10

Thalamic nuclei: Anterior nucleus: Memory. Projects to the cingulate gyrus. Receives connections from mammillary bodies via mammillothalamic tracts. Anterior nucleus or dorsomedial nucleus of thalamus may be affected in Wernicke-Korsakoff synd. Dorsomedial: Emotions, sleep-wake cycle, executive function. Receives input from prefrontal cortex & limbic structures. Major thalamic relay for info traveling to frontal association area. Ventral anterior: Motor control. Receives input from globus pallidus & projects to thalamus & frontal cortex. Ventral lateral: Motor control. Receives motor input from cerebellum & basal ganglia & projects to motor, premotor, & supplementary motor cortex. Ventral posterior medial & lateral: Relays sens info from face & body respectively to primary somatosens cortex. Medial geniculate: Relays auditory info from inf colliculus to transverse temporal (Heschl’s) gyrus. Lateral geniculate: Relays visual info from visual pathway to the calcarine cortex. Pulvinar: Modulates occipitotemporo-parietal cortical attention/visual processing. Reticular: Relays info between thalamic nuclei.

Question 11

Qual a vascularização do talamo?

Answer 11

Vascular supply of the thalamus:
Tuberothalamic artery: Arises from PCA.
Paramedian artery: Branch of basilar & PCA.
Posterior choroidal artery: Branch of P2 segment of PCA.
Inferolateral artery (aka thalamogeniculate artery): From P2 segment of PCA.

Question 12

Quais as síndromes de lesões do talamo?

Answer 12

Lesions involving the thalamus & clinical manifestations: Dejerine Roussy synd: Thalamic pain synd w/ hemisens painful sensation. Korsakoff dementia: Degen of dorsomedial and anterior nuclei of thalamus, mammillothalamic tracts, mammillary bodies due to thiamine defi ciency → memory loss, confabulation. Lesions in thalamus cause a signifi cant variety of defi cits, depend on location; include hemisens loss, hemiparesis, abnormal mvmts, behav Δs, akinetic mutism, somnolence, changes in mood, apathy, memory disturb, neglect, defi cits in ocular motility, visual fi eld defi cits, & lang diffi culty/ aphasia.

Question 13

Qual a vascularização do cerebelo?

Answer 13

Vascular supply to cerebellum: Sup cerebellar artery (SCA): Sup portion. Anterior inf cerebellar artery (AICA): Middle portion. Posterior inf cerebellar artery (PICA): Inf portion.

Question 14

Qual a anatomia do cerebelo?

Answer 14

Cerebellar anatomy: Cerebellar cortex: Three layers: molecular, Purkinje cell, granule cell. Cerebellar peduncles: Connect cerebellum to brainstem. Sup: Efferent pathway. Deep cerebellar nuclei send efferents in the superior cerebellar penduncles to synapse in t halamus; thalamocortical projections complete the cerebellar-cerebral feedback circuit. Middle: Afferent pathway. Fibers from cortex & sup colliculus project to c erebellum via pons & middle cerebellar peduncle. Inf: Afferent & efferent. Efferents project to vestibular nuclei & reticular formation & afferent info from vestibular nuclei, spinal cord, & brainstem tegmentum. Deep cerebellar nuclei: Outputs from cerebellar cortex travel through deep nuclei to regulate upper motor neurons in cerebral cortex, brainstem, & spinal cord. Cerebellar nuclei from lateral to medial are dentate, emboliform, globose, & fastigial nuclei.
Integrates sens info & sends outputs to the cerebral cortex, brainstem, & spinal cord to coordinate mvmt. Lesions result in ataxia/irreg uncoord mvmts. Composed of vermis & two hemispheres. Vermis lesions → truncal ataxia; hemisphere lesions → limb ataxia. Ataxia is typically ipsi to the lesion. Cerebellar lesions may also result in ↓ intellectual function & cerebellar cognitive affective synd, characterized by ↓ executive function, diff w/ visuospatial ability, fl attened affect, & inapprop behav.

Question 15

Quais as sindromes de mesencefalo?

Answer 15

Clinical synds & localization points in midbrain: Claude’s: Third + contralat ataxia due to involv of CN III & rubrospinal tract. Weber’s: Third + contralat hemiplegia due to involv of CN III & corticospinal tract. Benedict’s: Third + contralat ataxia & hemiplegia. Top of the Basilar: See below. Parinaud’s: Dorsal midbrain: Supranuclear paralysis of vert gaze, impaired convergence, convergence retraction nystagmus, light-near dissoc of pupils, Collier sign or lid retraction, skew deviation.

Question 16

Quais as sindromes de ponte?

Answer 16

Clinical synd & localization points in the pons: Basis pontis: Anterior pons incl corticospinal tracts; may result in contralateral ataxic hemiparesis, dysarthria-clumsy hand, or pure motor hemiparesis. Millard-Gubler: Ventral pons affecting fascicles of VI, VII, & corticospinal tract → ipsi facial palsy, ipsi lateral rectus palsy, contralat hemiplegia. Foville: Pontine tegmentum affecting fascicles of CN VI, VII, PPRF, & the corticospinal tract → ipsi peripheral seventh, gaze palsy to ipsi side, contralat hemiplegia. Raymond: Ventromedial pons; affects VI, corticospinal tract. Raymond Cestani Chenais: Dorsal pons, cerebellum → ataxia & contralat hemisens loss. Marie Foix: Lateral pons → ipsi cerebellar ataxia, contralat hemiparesis, contralat hemisens loss. AICA/lateral pontine: See stroke synds. Locked in: Bilat ventral pons → quadriplegia, aphonia, impaired horiz eye mvmts although vert eye mvmts & blinking may be intact due to sparing of supranuclear oculomotor pathways; pt may be awake due to sparing of reticular formation.

Question 17

Quais as sindromes de bulbo?

Answer 17

Clinical synds & localization points in the medulla: Lateral medullary “Wallenberg”: due to PICA or vert artery infarct ipsi → facial numb, contralat body numb, ipsi ataxia, gait instability, N/V/vertigo, Horner synd, ipsi palate deviation. Medial medullary: Tongue deviation toward the side of the lesion, contralat paralysis of arm & leg, ↓ touch &
Greerproprioception contralat body. Hemiplegia cruciata: Crossed motor h emiparesis; paralysis of ipsi arm & contralat leg due to lower medullary lesion compromising crossed fi bers to arm & uncrossed fi bers to leg

Question 18

Quais as sindromes do I par craniano?

Answer 18

I: Olfactory nerve: Smell. May be damaged due to head injury, tumors, neurodegenerative dz. Foster-Kennedy synd: Tumor/mass lesion compressing olfactory bulb & optic nerve causing ipsi anosmia & optic atrophy & contralat papilledema.

Question 19

Quais as sindromes do II, III, IV e VI pares cranianos?

Answer 19

II: Optic nerve: Vision; afferent pupillary light refl ex. III: Oculomotor nerve: Motor: Innervates sup, medial, & inf rectus, inf oblique, levator palpebrae supis muscles. Autonomic: Efferent pupillary light refl ex; accommodation of lens. Clinical synds & localization points involving the third nerve: INO (internuclear ophthalmoplegia): due to MLF lesion; ipsi adduction paresis w/ contralat abducting nystagmus. WEBINO (wall-eyed bilat INO): due to midbrain lesion involving both medial recti & both MLFs. Common in MS. One & a half synd: MLF + PPRF or MLF + sixth nuclear lesion causing ipsi adduction paresis w/ gaze deviation to ipsi side, w/ only mvmt being contralat abducting nystagmus. Horner synd: Clinical fi ndings: Classic triad: Ptosis, miosis, anhidrosis. Other possible fi ndings: (1) “upside down ptosis” due to sympathetic denervation to the lower eyelid retractors, (2) heterochromia iridis (diff in eye color b/w two eyes) in congenital causes, and (3) apparent enophthalmos. First order neurons: Descend from hypothalamus to intermediolateral cell column (ILC) at C8–T2. Second order neurons (preganglionic): Ascend from ILC through cervical sympathetic chain over lung apex, then along common carotid artery to synapse at sup cervical ganglion. Third order neuron (postganglionic): Travels w/ carotid artery up cavernous sinus to form nasociliary branch of trigeminal nerve & reaches eye as long & short ciliary nerve. Dx: If Horner’s present, cocaine fails to dilate pupil. (Cocaine blocks reuptake of norepinephrine.) Hydroxyamphetamine dilates a miotic pupil if lesion is fi rst or second order, but not if lesion is third order. (Hydroxyamphetamine causes release of norepinephrine from intact nerve endings.) Orbital apex: CN II, III, IV, VI, V1, proptosis. Sup orbital fi ssure synd: CN III, IV, VI, & V1. Cavernous sinus synd: CN III, IV, VI, V1, V2, & sympathetics. IV: Trochlear Nerve: Motor: Innervates sup oblique muscle. Depresses eye when adducted or intorts eye when abducted. Bielschowsky sign: Head tilt to side of weak sup oblique increases diplopia.
VI: Abducens Nerve: Motor: Innervates lateral rectus muscle; abducts eye

Question 20

Quais os ramos sensitivos do trigemio?

Answer 20

V: Trigeminal Nerve: Motor: Innervates muscles of mastication. Sens: Three divisions: V1: Forehead, corneal, eyelids, nose, scalp; V2: Nose & cheeks, upper gums, nasal cavity; V3: Chin, lower jaw & teeth, cheek, anterior tongue.

Question 21

Quais as síndromes do nervo facial?

Answer 21

VII: Facial Nerve: Motor: Motor branches exit from stylomastoid foramen to innervate facial muscles involved in mvmts & expression. Motor branches also innervate the stapedius & dysfxn leads to hyperacusis. Sens: (nervus intermedius) supplies taste in anterior 2/3 of tongue & sensation of acoustic meatus. Autonomic: Autonomic branches (greater petrosal nerve, chorda tympani) supply glands for lacrimation & salivation. Clinical synds & localization points involving the seventh nerve: Supranuclear lesion: Contralat facial wkns w/ sparing of the forehead, due to bilat supranuclear innervation of forehead. Nuclear or fascicular lesion: Ipsi wkns of face & forehead. Cerebellopontine angle lesions (e.g., meningiomas, schwannomas) & lesions of meatal segment of the facial nerve: Ipsi peripheral facial nerve palsy incl loss of taste over ipsi anterior 2/3rds of tongue w/o hyperacusis due to assoc eighth CN palsy w/ ipsi tinnitus, deafness & vertigo. Geniculate ganglion lesions (Ramsay Hunt synd-latent VZV): Facial palsy of LMN type w/ hyperacusis & loss of taste assoc w/ geniculate neuralgia & herpetic vesicles in ear drum, external auditory meatus or palate. Lesions proximal to nerve to stapedius: Hyperacusis along w/ ipsi facial wkns & loss of taste. Lesions proximal to the greater petrosal nerve: Impaired lacrimation. Gradenigo synd: Lesion of CN VI & VII w/ retroorbital facial pain due to lesion in petrous apex (may be compl of otitis media/ mastoiditis & nasopharyngeal carcinoma). Lesions at or distal to stylomastoid foramen: Isolated facial motor paralysis w/o hyperacusis or impaired taste/ lacrimation. Aberrant regeneration of seventh nerve: Causes crocodile tears or Bogorad synd; gustatory sweating or Frey synd.

Question 22

Quais as sindromes do VIII par? Quais as caracteristicas de uma vertigem central?

Answer 22

VIII: Vestibulocochlear nerve: Sens: Equilibrium & hearing. Composed of vestibular & cochlear nerves. Cochlear nerve: Defi cits result in tinnitus, deafness. Vestibular nerve: Vertigo: Often positional (see table below); Nystagmus: vert/horiz/ rotatory; General sx: Diaphoresis, nausea, vomiting, tachycardia, hypotension.
# Central Lesion:
- Severity Less intense
- Continuous
- Positional No (usually)
- Nauseausually present but may be less pronounced
- Direction of nystagmus vert Horiz, torsional, vert, may be variable
- Intensity of nystagmus Unaffected by fixation and Not fatigable Neurologic Absent Latency before onset of nystagmus/vertigo
- Neurologic sx: present usually

Question 23

Quais as síndromes de pares cranianos bulbares?

Answer 23

IX: Glossopharyngeal nerve: Motor: Palate elevation, swallowing. Sens: Taste in posterior 1/3 of tongue, palate sensation. Autonomic: Parasympathetic innervation to parotid gland. Jugular foramen synd: Involvement of CN IX, X, XI due to mass lesion or compression of jugular foramen. X: Vagus nerve: Motor: Palate elevation, swallowing, innervation of vocal cords. Sens: Epiglottis and laryngeal sensation. Autonomic: Parasympathetic innervation to trachea, GI tract, heart. XI: Spinal accessory nerve: Innervates trapezius & sternocleidomastoid, responsible for shoulder shrug, neck mvmt. XII: Hypoglossal nerve: Motor: Tongue mvmt.

Question 24

Qual a vascularização da medula espinhal?

Answer 24

Vascular supply of the spinal cord: Upper (cervicothoracic) region: Supplied by ant spinal artery & artery of cervical enlargement arising between C4 & C8. Intermediate (midthoracic) region: Supplied by branches of intercostal arteries. Also known as watershed of the spinal cord. Lower (thoracolumbosacral) region: Supplied by ant radicular artery of Adamkiewicz.

Question 25

Quais as sindromes medulares?

Answer 25

# Mielopatia transversa:  Motor: LMN wkns at level, UMN wkns below level Sens: Loss of pain, temperature, vibration, proprioception, & touch, two to three segments below level, hyperesthesia/pain at the level Reflexes: Hyporeflexia at the level, hyperreflexia below the level
# Sd de Brown-Sequard: Motor: LMN wkns at level, UMN wkns below level Sens: Ipsi loss of proprioception, vibration & touch below the level, contralat loss of temperature & pain two to three segments below the level; ipsi hyperesthesia at the level of the lesion Refl exes: Ipsi hyporefl exia at the level & hyperrefl exia below the level
# Sindrome cordonal anterior: Motor: LMN wkns at the level of lesion Sens: Pain & temperature loss below the lesion (intact light touch, vibration, & proprioception) Refl exes: Hyporefl exia at the level of lesion
# Sindrome cordonal central:Motor: Wkns at the level. May cause a “man in the barrel synd” if at the cervical level Sens: Cape distribution of pain & temperature loss Refl exes: Hyporefl exia at the level

Question 26

Como diferenciar sindrome de cone medular e sindrome da cauda equina?

Answer 26

• Sd de cone medular: Due to lesion of conus medullaris Sx: Flaccid LE paralysis, urinary retention & decreased anal tone, variable sens loss but more often symmetrical, saddle anesthesia, diminished ankle refl exes, UMN & LMN fi ndings. Causes: Spinal stenosis, trauma, herniated disc, abscess, neoplasm, hemorrhage, and vascular malformation
• Sd de cauda equina: Lesion of lumbar & sacral roots below L3 Sx: Asymmetric & fl accid wkns of LE, urinary retention (later fi nding), asymmetric sens loss, which may be in a radicular pattern, saddle anesthesia, knee & ankle refl exes often absent, LMN fi ndings. Causes: Herniated disc, epidural compression from bony collapse, epidural hematoma, meningeal carcinomatosis meningitis, tumors, trauma, and infection

Question 27

Quais as vias de circulação liquorica que podem, na obstrução, causar hidrocefalia?

Answer 27

CSF fl ow: Produced by choroid plexus & flows from lateral ventricles → Foramen of Monro → third ventricle → aqueduct of Sylvius → fourth ventricle → foramen of Luschka (lateral) & Foramen of Magendie (midline) → subarachnoid space.

Question 28

Como é a anatomia venosa do sistema nervoso central?

Answer 28

A. Superior sagittal sinus B. Inferior sagittal sinus C. Straight sinus D. Confl uence of sinuses E. Transverse sinus F. Sigmoid sinus G. Superior petrosal sinus H. Inferior petrosal sinus I. Cavernous sinus J. Internal jugular vein K. Ophthalmic veins L. Basal vein of Rosenthal M. Great cerebral vein of Galen

Question 29

Quais as síndromes de AVEs de circulação anterior?

Answer 29

# Artéria Cerebral Média: Wkns & sens loss of contralat face, arm, & to lesser degree leg, dysarthria, global aphasia and apraxias in dominant hemisphere, neglect in nondominant hemisphere. Homonymous hemianopsia. Gaze deviation (looking toward lesion). Sup division: Supplies rolandic & prerolandic areas. Dense sensorimotor defi cit involv contralat face, arm & to lesser extent leg. Deviation of eyes toward lesion. If dominant side: initial global aphasia which changes to Broca aphasia, or Broca aphasia from outset. Inf division: Supplies lateral temporal & inf parietal lobes. If dom side, causes Wernicke aphasia. Sup quadrantanopia or homonymous hemianopia. For R sided lesion: left sided visual neglect & other signs of amorphosynthesis, agitated confusional state may occur w/ temporal lobe damage. 
# Artéria  Cerebral Anterior: Contralat leg wkns & sens loss. If both ACAs involved, may have bilat paraparesis, abulia, gegenhalten (paratonic rigidity), contralat grasp, & urinary incont. 
# Arteria Coroidea Anterior: Supplied internal segment of globus pallidus & posterior limb of internal capsule & contiguous structures. Contralat hemiplegia, hemihypesthesia, homonymous hemianopsia.

Question 30

Quais as sindromes de circulação posterior?

Answer 30

# Artéria Cerebral Posterior: Precommunal PCA (P1): Infarct often involves P1 perforators to midbrain, subthalamus, & thalamus (see below). Postcommunal PCA (P2): Cortical temporal & occipital lobe signs, hemianopia w/ macular sparing, memory disturbances. Dominant occipital lobe + splenium of the corpus callosum: Alexia w/o agraphia. Visual agnosia for faces, objects, mathematical symbols, & colors. Peduncular hallucinosis: Highly vivid visual hallucinations due to lesions of midbrain/tegmentum. Anton synd. Balint synd. Palinopsia. 
# Artéria Cerebral Superior: Ipsilateral upper & lower extremity dysmetria, dysarthria, gait ataxia, & nystagmus. Variable vertigo, nausea, vomiting & headache. Basilar artery: Branches supply pons & sup cerebellum. Small vessel perforators include paramedian, short circumferential, long circumferential. 
# Sindrome de Topo de Basilar: (1) somnolence/altered mental status, (2) lid retraction/Collier sign, (3) akinetic mutism, (4) peduncular hallucinations, (5) ptosis, d/os of ocular mvmt, paralysis of vert gaze, (6) convergence retraction nystagmus; pseudo-abducens palsy, and (7) skew deviation.
# Artéria Cerebelar Antero-Inferior (AICA): Supplies lateral pons, middle cerebellar peduncle, anterior cerebellar hemispheres, CN VII & VIII.  Stroke may lead to hearing loss & facial palsy together with ipsilateral limb dysmetria, gait ataxia, nausea, vomiting & vertigo. 
# Artéria vertebral: Arise from subclavian arteries proximally, join distally to form basilar. Four segments: V1: From subclavian artery to C6; V2: From C6–C2; V3: From C2 to atlanto-occipital joint; V4 (intradural segment): Pierces dura at foramen magnum to enter intracranial cavity, travels to pontomedullary junction, where they merge to form basilar. Occlusion → brainstem or cerebellar dysfunction. Sx include limb or truncal ataxia, nystagmus, ipsi Horner synd, ipsi light touch & proprioception, contralat pain & temp sensation, ipsi tongue deviation, hemiparesis, INO, lateral medullary synd (see below). 
# Artéria Cerebelar Postero-inferior (PICA): Supplies inf and posterior aspects of cerebellar hemispheres & inf vermis. PICA strokes p/w headache & vestibular sx of n/v & vertigo; cognitive & affective changes can occur. If anterior lobe is spared then dysmetria & ataxia may be  mild or absent. Cerebellar posterior lobe edema from PICA infarcts can lead to herniation & brainstem compression. PICA lesions may cause lateral.

Question 31

Quais as síndromes lacunares?

Answer 31

Selected small vessel/lacunar syndromes: Hemisens loss & hemiparesis: Thalamocapsular. Pure hemisens loss: Thalamus. Pure motor hemiparesis: Internal capsule, corona radiata, & basis pontis. Dysarthria/clumsy hand: Genu of the internal capsule & basis pontis. Ataxic hemiparesis: Pons, midbrain, or internal capsule, or parietal white matter