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64 Cards in this Set
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major ventromedial brainstem tracts: reticulospinal: integration centers, major sensory inputs detecting postural instability, integration of sensory inputs |
integration centers= pontine and medullar reticular formation; major sensory inputs detecting postural instability; integration of sensory inputs= integration of proprioceptive input to maintain balance and posture |
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major ventromedial brainstem tracts: tectospinal (or colliculospinal): integration centers, major sensory inputs detecting postural instability, integration of sensory inputs |
integration centers= deeper layers of superior colliculi; major sensory inputs detecting postural instability= eyes and ears; integration of sensory inputs= integration of visual and auditory stimuli for involuntary orientation of the head and eyes |
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major ventromedial brainstem tracts: vestibulospinal: integration centers, major sensory inputs detecting postural instability, integration of sensory inputs |
integration centers: vestibular complex; major sensory inputs detecting postural instability= vestibular system; integration of sensory inputs= integration of vestibular input to maintain balance and posture |
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trace the tectospinal (or colliculospinal) tract |
ventromedial tract; IPSILATERAL cortical input; DECUSSATES in posterior (dorsal) tegmental decussation; TERMINATES CONTRALATERAL TO ORIGIN in upper cervical levels |
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trace the reticulospinal tract |
ventromedial tract; pontine (medial)= BILATERAL cortical input, does not decussate, TERMINATES IPSILATERAL TO ORIGIN; medullary (lateral)= BILATERAL cortical input, BILATERAL termination |
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trace the vestibulospinal tract |
ventromedial tract; lateral= somatotopically organized, does not decussate, TERMINATES IPSILATERAL TO ORIGIN AND TERMINATION IS IN THE CERVICAL REGION OF THE SPINAL CORD; medial= BILATERAL termination limited to cervical spinal cord segments |
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trace the rubrospinal tract |
dorsolateral tract; IPSILATERAL cortical input; DECUSSATES in the ANTERIOR (VENTRAL) TEGMENTUM; TERMINATES CONTRALATRAL TO ORIGIN |
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balance and posture determined by the tone of what musculature? |
axial, flexor, and extensor musculature |
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rubrospinal tract: actions on muscle groups |
facilitates upper limb flexor and inhibits extensor alpha and gamma motor neurons to the upper extremities; BIAS FOR UPPER LIMB FLEXORS |
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tectospinal tract: actions on muscle groups |
orienting movements of head and eyes |
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medial vestibulospinal tract: actions on muscle groups |
inhibits extensors and neurons innervating muscles of the back and neck |
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lateral vestibulospinal tract: actions on muscle groups |
supplements the excitatory function of the pontine (medial) reticulospinal system by integrating vestibular info; EXTENSOR BIAS |
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pontine (medial) reticulospinal tract: actions on muscle groups |
excites upper and lower proximal limb extensor and inhibits flexor alpha and gamma motor neurons, excites antigravity muscles; facilitates extensor spinal reflexes, increases muscle tones of axial and proximal muscle; EXTENSOR BIAS |
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medullary (lateral) reticulospinal tract: actions on muscle groups |
inhibits extensor and excites flexor alpha and gamma motor neurons, inhibits antigravity muscles; suppresses extensor spinal reflex activity; decreases muscle tone and axial and proximal muscle |
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lesions of descending brainstem motor tracts |
essentially never see isolated lesions of ONLY rubrospinal, vestibulospinal, tectospinal, and reticulospinal fibers; lesions of corticospinal tract (indirect pathways) to brainstem motor nuclei --> POSTURING appears --> DECORTICATE (upper limb flexion with lower limb extension) and DECEREBRATE POSTURING (upper and lower limb extension) |
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clinical correlation: posturing |
generally descending cortical tracts projecting to motor brainstem sites impose an INHIBITORY TONE on the 'bias' action of motor brainstem tracts; therefore lesions of these descending cortical tracts can lead to DISINHIBITION of descending brainstem motor tracts; POSTURING is a sign of this disinhibition following brain injury (so expression of the usually repressed bias); since posturing is an important indicator of the amount of damage that has occurred to the brain it is used to assess the severity of head injury on the GLASGOW COMA SCALE |
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head injury classification: glasgow coma sclae |
severe= 8 or less; moderate= 9-12; mild= 13-15 |
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what is going on in decorticate posturing |
lesion above the red nucleus (midbrain); an upper motor neuron syndrome posturing that involves rigidity, flexion of the arms, clenched fists, and extended legs; tonic neck reflexes can occur= aka fencing reflex observed in infants, when the child's head is turned to the site the arm on that side will straighten and the opposite arm will bend, if the reflex is observed in adults or in the infant past 6 months of age a disorder of the upper motor neuron may be present |
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what is going on in decerebrate rigidity |
lesion below the red nucleus (midbrain); occurs when the posterior part of the brain stem and spinal cord are isolated from the rest of the brain by injury at the superior border of the pons; the extensor muscles in all of the limbs and those of the trunk and neck have increased tone; when the brain stem is transected inhibitory influences from the cortex and basal ganglia can no longer reach the spinal cord and facilitatory influences which descend in the vestibulospinal and reticulospinal tracts dominate; this results in increased activity of alpha motor neurons innervating extensor muscles which can be due to increased gamma motor nueron discharge for these muscles |
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decorticate posturing and decerebrate posturing at the same time? |
decerebrate posture can occur on one site, on both sides, or in just the arms; it may alternate with decorticate posture (abnormal posturing due to corticospinal tract injury) or a person can have decorticate posture on one side and decerebrate posture on the other |
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sites and causes of posturing: decorticate |
in the diffuse hemisphere region; trauma, ischemia, hypoglycemia/other metabolic disorders, infection, drugs |
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sites and causes of posturing: decerebrate |
in the bilateral thalamic region, brainstem compression; hemorrhage, infarction, supra or infra tentorial mass lesions; ischemia, hemorrhage, drugs |
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summary: posturing and coma |
normally corticospinal input tonically inhibits brainstem motor centers and associated POSTURAL REFLEXES; lesion of corticospinal tract results in DISINHIBITION of brainstem motor centers resulting in the UMN sign of POSTURING= a lesion above the red nucleus results in DECORTICATE POSTURING OR FLEXOR SPASTICITY, a lesion that extends to include the red nucleus results in DECEREBRATE POSTURING OR EXTENSOR SPASTICITY; coma= pathological state of unconciousness from which a person cannot be aroused to make purposeful responses, as a rule LIGHT coma is present when reflex motor response (i.e. decorticate and decerebrate posturing) can be elicited by NOXIOUS stimulation, in DEEP coma there is no response |
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origins of pyramidal tract fibers |
PRIMARY MOTOR CORTEX brodman's area 4, MI lowest current threshold elicits contralateral movement= BETZ cells have largest somas in CNS and are a subset (5%) of primary motor cortex pyramidal neurons in area 4, MIRROR cells respond to performance of action/observation of action in others; MEDIAL AND LATERAL PROMOTOR CORTEX= immediately rostral to precentral gyrus, medial supplemental motor area (SMA), lateral premotor cortex (PMC), brodman's area 6, MII higher threshold often elicits bilateral limb movement; PRIMARY SOMATIC SENSORY CORTEX= also called S1, areas 3, 1, 2 especially 3z that receives input from muscle spindles |
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primary motor cortex |
primary motor cortex neurons fire 5-100 msec before the onset of a movement; organizes voluntary and fine control of distal musculature via DIRECT PATHWAY; primate evolution= an increase in the overall size of the corticospinal tract especially to the musculature of the digits, one hypothesis is foveate retina/fine motor control; primary motor cortex encodes for= force of a movement, direction of movement, extent (distance) of movement, speed of movement |
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direct corticospinal pathways |
lateral corticospinal tract= 90% of fibers, notable for synaptic contacts DIRECTLY onto alpha motor neurons, damage results in a permanent loss of the fine control of the digits; anterior cotricospinal tract= 10% of fibers, responsible for the voluntary control of the proximal limb and axial musculature, terminates bilaterally |
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direct corticobulbar/corticospinal pathways: genu/posterior limb of internal capsule |
convergence of all ascending and descending white matter tracts to and from the cortex; the descending motor fibers for the face, arm, and leg run medially to laterally in the posterior limb of the IC; blood supply to posterior limb of IC= lenticulostiate branches of MCA, anterior choroidal artery of internal carotid artery; clinical note= LACUNAR INFARCTS arise from blocked blood flow to small, deep, penetrating vessels, one common location is the internal capsule white matter |
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indirect corticospinal pathways |
cerebral motor cortical output is mostly inhibitory to spinal cord reflexes via indirect pathways; for this reason interruption of corticospinal results in HYPERREFLEXIA |
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major spinal terminations of CST fibers |
lamina VII, intermediate zone= presynaptic inhibition of primary afferent fibers such as I1 afferents from stretch receptors, inhibition of reflexes during normal gait probably by presynaptic inhibition of Ia afferents; lamina IX motor nuclei= in primates substantial direct corticospinal projections to alpha and gamma motor neurons in lamina IX, also synaptic contact mainly with short interneurons that synapse upon alpha and gamma motor neurons |
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somatotopic representation in primary motor cortex |
the PRIMARY MOTOR CORTEX or M1 is located on the PRECENTRAL GYRUS and on the ANTERIOR PARACENTRAL LOBULE on the medial surface of the brain; paracentral lobule refers to the junction of the precentral gyrus and postcentral gyrus on the medial surface of the cerebral cortex and contains the sensorimotor representation of the distal lower extremities |
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stimulation of a single primary motor cortical neuron elicits muscle activity |
primary motor cortex= comparatively low threshold, monosynaptic connections to a few spinal motor neurons, projects to contralateral side |
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motor functions of premotor cortex |
stimulation of premotor areas= high threshold, coordinated contractions at more than one joint; medial (dorsal) premotor cortex= supplemental motor area (SMA), active with initiation of movement from internal cues; lateral (ventral) premotor cortex= active at appearance of external cue |
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lateral premotor cortex generates potentials in response to what |
the external cue; the LATERALIZED PREMOTOR POTENTIAL OR READINESS POTENTIAL is a measure of electrical activity that precedes voluntary muscle movement; the readiness potential precedes voluntary acts by about half a second; voluntary acts are nonconsciously initiated |
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medial (dorsal) premotor cortex is activated from what |
memory of motor activity; more complex finger PERFORMANCE; finger REHEARSAL or motor imagery; SUPPLEMENTARY MOTOR AREA (SMA) is heavily activated while the primary motor cortex and somatosensory cortex are not because the fingers weren't actually moving |
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motor strategies for maintenance of balance and posture |
HIERARCHICAL ORGANIZATION of DIRECT AND INDIRECT motor pathways; FEEDBACK and FEEDFORWARD (anticipatory) mechanisms; feedforward mechanisms= LEARNED ADAPTIVE POSTURAL CONTROL, FEEDFORWARD PREACTIVATION of muscle groups; HE RAN OUT OF TIME HERE |
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motor strategies for maintenance of balance and posture |
feedback response= a muscle activation pattern that is a response to the sensory signals resulting from postural instability; feedforward (anticipatory) response= activity of trunk and limb muscles that occurs before voluntary movement to prepare the body for any disturbance to posture, feedforward responses can originate from motor cortex |
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indirect motor pathways modulate what |
flexor/extensor muscle tone and reflexes; for intact walking ventral CST projects to reticulospinal neurons to the medullary (lateral reticulospinal tract (activates flexor reflexes, inhibits extensor reflexes) and the pontine (medial) reticulospinal tract (activates extensor reflexes, inhibits flexor reflexes) |
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learned adaptive postural control and feedforward reflex modulation |
HE MADE A POINT OF STILL DOING THIS ONE; stretch reflex sensitivity can be increased or decreased; initially feedback then feedforward postural adjustment; modulation of stretch reflex by central descending mechanisms; adaptive postural control requires intact cerebellum= atrophy of anterior cerebellar lobe prevents appropriate SCALING of correcting postural response, all levels of CNS are involved in postural control (integrity of brainstem centers is necessary for generation of compensatory postural adjustments, integrity of highest levels of the CNS including the motor areas of the cerebral cortex is necessary for anticipatory postural adjustments, adaptive postural control requires an intact cerebellum) |
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feedforward preactivation of muscle groups for maintenance of body posture |
motor cortex -- direct pathways corticospinal tract --> contract bicep; indirect pathway --corticoreticular tract--> brain stem reticular formation --reticulospinal tracts (postural set automatic postural adjustment)--> preactivated contraction of gastrocnemius; POSTURAL SET is a task specific feedforward motor readiness to respond as would occur with a runner getting set on their mark |
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central pattern generators (CPGs) |
a set of neural circuit capable of producing repetitive activity in the absence of any sensory input; CPGs possess rhythmic predetermined neural activation for activities such as breathing, chewing, and walking; they free up your conscious mind sot hat you don't have to send down a voluntary command every time you want to put one foot in front of the other |
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spinal CPGs controlling locomotion |
CPG activity for rudimentary walking can be elicited from an isolated human spinal cord; electrical stimulation of the lumbar spinal cord in paraplegics can induce rhythmic, alternating stance and swing phases; in intact human direct and indirect pathways converge on CPGs |
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definition of a stroke |
any disease that disrupts blood flow to a focal region of the brain; 80% ischemic= thrombosis which is a blood clot at the site of origin and most common or Embolism which is a blood clot that Enters from a distant site; 20% hemorrhagic |
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brainstem syndromes involving the pyramidal tract |
three medial brainstem syndromes (oculomotor, abducens, and hypoglossal) (the alternating hemiplegias) and locking in syndrome |
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the rule of 4 of the brainstem |
NTD |
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medial inferior midbrain: weber's syndrome |
aka superior alternating hemiplegia; midbrain= base cerebral peduncle (crus cerebri); paramedian branches of posterior cerebral artery (PCA); presentation= pyramidal tract contralateral hemiparesis of the limb and facial muscles, CN III (oculomotor) ipsilateral oculomotor palsy, eyes deviate laterally due to medial rectus muscle weakness (diplopia), ptosis (low eyelid), parasympathetic branch of CH III ispilateral failure of pupil constriction in response to light pupil is dilated and fixed |
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medial inferior pontine syndrome: foville's syndrome |
aka middle alternating hemiplegia; pons basis pontis; paramedian branches of basilar artery; presentation= pyramidal tract contralateral hemiparesis upper and lower extremity, CN 6 abducens ipsilateral lateral rectus palsy and diplopia |
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medial medullary syndrome: dejerine syndrome |
aka inferior alternating hemiplegia; penetrating branches of the vertebral or anterior spinal artery; presentation= pyramidal tract contralateral hemiparesis upper and lower extremity, CN 12 ipsilateral tongue weakness +/- atrophy tongue points to side of lesion, medial lemniscus vibration and proprioception |
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summary: differentials for alternating hemiplegias |
medial inferior midbrain= weber's sundrome, superior alternating hemiplegia (contralateral hemiparesis, ipsilateral oculomotor (CNIII) palsy); medial inferior pontine syndrome= foville's syndrome, middle alternating hemiplegia (contralateral hemiparesis, ipsilateral abducens (CN4) palsy; medial medullary syndrome= dejerine syndrome, interior alternating hemiplegia (contralateral hemiparsis, ipsilateral hypoglossal (CN12) palsy |
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locked in syndrome |
ventral pontine syndrome; pons bilateral ventral medial pons; basilar artery; pyramidal tract= corticospinal tract complete paralysis from head to toe, corticobulbar tract complete paralysis of entire face aphonia, spares the oculomotor and trochlear nerves so pt is only able to communicate with eye movements, pt is awake and aware |
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blood supply to motor cortex |
anterior cerebral artery (ACA) supplies the medial cortex (lower extremity of homonuculus); middle cerebral artery (MCA) supplies the lateral aspect |
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distribution of middle cerebral artery (MCA) occlusions |
NTD |
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lenticostriate/anterior choroidal arteris |
posterior limb of internal capsule, subcortical structures are fed by: MCA --> lenticulostriate artery, internal carotid artery --> anterior choroidal artery; HX chronic HTN in 80-90% of cases; lacunar strokes; lacunar syndrome= pure motor hemiplegia, face, arm, and leg, no cortical signs or sensory deficits; anatomical location= posterior limb of internal capsule, corona radiate, pons (basis postis) |
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anterior cerebral artery (ACA) |
most common presentation= contralateral weakness, contralateral hemisensory loss; foot/leg>trunk, mild or no involvement of upper extremity |
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transcortical motor aphasia |
NTD |
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how can you tell whether the stoke is subcortical (i.e. internal capsule) or cortical? |
a pt who presents with arm and leg weakness may have either a small internal capsule stoke or a large ACA+MCA cortical stoke; the presence of these cortical signs exclude an internal capsule stroke= gaze preference or gaze deviation, expressive or receptive aphasia, visual field deficits, visual or spacial neglect |
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A 74 y/o woman with a history of hypertension suddenly displays with LOC. Sometime later, the pt displays with weakness of her left face, including upper and lower limbs, weakness of her face, and slurred speech. The diffusion weighted MRI of this pt is shown here, in which the high signal reflects vascular occlusion of a region of the brain. Which of the following best characterizes what happened to this pt? a. a stroke involving the right anterior cerebral artery b. a stroke involving the right middle cerebralartery c. occlusion of the right anterior communicating artery d. occlusion of the right posterior communicating artery e. a stroke involving the posterior cerebral artery |
B |
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A pt who suffered a stroke presents with a paralysis of the right side of the lower face, right spastic paralysis of the limbs, and deviation of the tongue to the right with no atrophy. Which of the following structures was most likely affected by the stroke? a. internal capsule of the right side b. internal capsule of the left side c. base of the medulla on the right side d. base of the medulla on the left side |
B |
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An 81 y/o right handed woman with a HX of hypertension was brought to the ER by her family one morning when she was suddenly ‘unable to communicate properly’ speaking with words and sentences that did not make any sense. On PE she has an irregular pulse and spontaneous speech was fluent with normal prosody and grammatical constructions however most of what she said was meaningless and did not fit the context. She followed no commands except to close her eyes. Did not raise her arms when asked. Where is the lesion? a. left MCA inferior division b. left MCA superior division c. left lenticulostriate artery d. right MCA inferior division e. right MCS superior division |
A |
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A 59 y/o male suffered a stroke and later presented with a spastic paralysis. Which of the following structures affected by the stroke most likely accounts for the spasticity? a. ventral horn cells b. corpus callosum c. postcentral capsule d. internal capsule e. substantia nigra |
D |
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a 7 y/o chinese boy with a history of bronchial asthma had upper respiratory tract infection for the preceding 2 weeks treated by a pediatrician. He then presentedwith confusion and incoherent speech on the day of admission. About 12 hrs after admission, he developed generalized tonic convulsions progressing to posturing. He succumbed on the 4th day to hospitalization. MRI on the 3rd day showed severe cerebral edema with diffuse bilateral and symmetrical lesions in the deep white matter of the cerebral hemispheres. Which type of posturing would be expected? a. decorticate b. decerebrate |
A |
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An 84 y/o male pt with a past medial history of atrial fibrillation and abnormal glucose tolerance, presented with sudden right leg motor deficit. It is likely this pt has an occlusion of both: a. anterior cerebral arteries (ACA) b. posterior cerebral arteries (PCA) c. middle cerebral arteries (MCA) |
A |
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A 48 y/o woman presented with a sudden change of consciousness. On the Glasgow scale the best verbal response was 1 (no response) and the eye opening response was 1 (no response). The best motor response was 2. The brain CT showed a rostral pontine hemorrhage. A mechanical ventilator wasused to support her respiration. This pt likely exhibits a posture of: a. upper limb flexion, lower limb extension b. flexion of all 4 limbs c. extension of all 4 limbs d. upper limb extension, lower limb flexion |
C |
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A 58 y/o hypertensive truck driver presents with complaints of weakness and numbness on the left side of his body and of slurred speech. Your exam reveals paralysis ofthe left hand and brisk reflexes in the left arm and leg. There is decreased sensation to vibration on the left side of his body. The cranial nerve exam is normal except that when asked to protrude his tongue it deviates to the right. An MRI would most likelyreveal a vascular lesion in the: a. right ventral medulla b. right ventral pons c. right ventral midbrain d. right internal capsule e. right cerebral cortex |
A |
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Neurons of the primary motor cortex are characterized by their: a. comparatively low threshold for muscle activation b. polysynaptic connections to spinal motor neurons c. robust projection to ipsilateral spinal motor neurons d. comparatively high threshold for muscle activation e. activation in response to external cues |
A |