184 terms

Bio of the Brain Exam 3


Terms in this set (...)

Cortical layers
1. layer 1- molecular, few cells
2. layer 2-3 - granular and small pyramidal neurons, cortical association
3. layer 4- small granular cells, major thalamic termination layer
4. layer 5- large pyramidal cells, main output layer to many structures
5. layer 6- polymorphic cells, main output to thalamus
During initial brain development
1. growth of axonal and dendritic branches
2. elimination of some not needed synapses
- in adult brain these go together with modulation from environment, through sensory and motor abilities, social interactions, and cognitive behavior
Critical period
-time when experience and neuronal activity that reflects that experience have maximal effect on acquisition of skilled execution of particular behavior
- failure to be exposed to appropriate stimuli will not be able to be compensated, long lasting consequences
-most animals behavior repertoire depends on patterns of connectivity established during development- built in behaviors
- parental imprinting: hours, day
-sensorimotor skills: longer window
-periods of pronounced brain plasticity (reorganization ability)
Built in behaviors
modified by environment through experience especially during temporal window (critical period), where maximal effects of experience could be observed
Imprinted behavior is _
Bonding in mammals depend initially on _ and _
olfactory and gustatory cues
Language acquisition critical period
-language develops readily between age 5-puberty
-final retirement of language in puberty (end of critical period)
-after that language acquisition it is much more difficult and ultimately less successful
-in 50s and 60s: observed that children who experience brain injury early in life develop far better language skills than adults with similar injuries
Hebb's postulate
-coordinated activity between a presynaptic terminal and postsynaptic neuron strengthens the synaptic activity between them
- competition: more active groups will win
-cooperation (or correlation): synchronized inputs strengthen together
Critical period in visual system development
-Hubel and Wiesel
-deprivation of sensory input easy to study in eyes
-suturing eyes in different period of development
-ocular dominance circuitry: ex. of activity dependent plasticity
1. radioactive amino acids injected in eye
2. transynaptic transport through the LGN terminates in layer 4 of primary visual cortex
3. terminations are visible as bright bands on autoradiogram
-monocular deprivation in kittens: most cells activated in eye open
-monocular deprivation in adult: most cells active in eye that was closed
Cortical blindness
ambylopia is permanent
Critical period of 6 days in kittens
-eye opened at postnatal day 7
-3 days was enough to produce effect
-6 days produce the same shift in 2.5 months deprivation
Monkeys-initial experience-independent segregagtion
-spontaneous activity in retina
-one eye was injected with radioactive tracer
- in monkeys striations in the cortex (ocular dominance columns) present at birth without visual experience, suggesting that there is a segregation of LGN axons from thalamus t cortex
Monocular deprivation during critical period
-alters anatomical connections from thalamus to layer 4
-Synaptic inputs from the non-deprived eye ( white, coming to cortex via the the thalamus) are greatly expanded at the expense inputs from the deprived eye- competitive interactions between eyes
-When both eyes are closed, input representation on visual cortex is closer to normal than in case of monocular deprivation
-Balance of inputs from both eyes is critical
-Competitive imbalance of inputs is the reason for different pattern of ocular dominance columns after visual deprivation of one eye
Three-eyed frog
-example of competition between inputs for cortical space
-frog optic tectum only receives input from one eye: no competition between two eyes
-transplant third eye during larval development: experimentally create competition
Activity of NMDA receptors
-controls the segregation of correlated activity that leads to segregated patterns of synaptic input in frog optic tectum
-Actions potentials in thalamocortical inputs related to one eye are better correlated with each other than with the other eye
-If correlated inputs dominate over local postsynaptic terminals, that interaction will exclude uncorrelated
-How much correlation contributes to the OD columns arrangement?
-Create experiment where activity levels in both eyes are the same while correlations between eyes are altered
-Cutting off one eye muscle- lateral or medial rectus induces changes in correlation of activity from corresponding retinas-- Induce misalignment of eyes- strabismus
Lesion of III cranial nerve
Ipsilateral eye deviates laterally, since medial rectus is paralyzed and lateral rectus is unaffected-lateral strabismus- one eye move away from midline
Lesion of VI cranial nerve
Affected eye deviates medially, as action of unopposed medial rectus muscle (controlled by CN III)- medial strabismus- one eye move toward midline
Vision affected in strabismus
-When eyes are misaligned, the straight or straighter eye becomes dominant. The vision strength (acuity) of the straight eye remains normal because the eye and its connection to the brain are functioning as they should
-The misaligned or weaker eye, however, does not focus properly and its connection to the brain is not formed correctly
-If strabismus is left untreated, the brain will eventually suppress or ignore the image of the weaker eye, resulting in amblyopia (or "lazy eye," when an eye is unable to focus on details) or permanent vision loss
- Induced crossed eyes (strabismus) during the critical period can result in LOSS of binocular vision
-correlated activity from both eyes results in Gaussian distribution
-uncorrelated activity due to strabismus all layers are driven exclusively by one or the other eye
-example of uncorrelated activity of eyes
-caused by strabismus, lack of stereopsis, vision acuity
Crossed eyes
both eyes turned inward
Wall eyes
both eyes turned outward
Correction of misalignment
adjust length of extra ocular muscles in critical period
Neurons that_ together _ together
Prolong the Critical period
-in mice ocular dominance plasticity is initiated by the development of intracortical inhibitory interneurons
-reduction of inhibitory transmission disrupts ocular dominance plasticity
-early enhancement of inhibitory transmission promotes period of OD plasticity
Cortical plasticity
If IN progenitors are transplanted and cortical plasticity
was assessed, 33-35 days after transplantation (that correspond to timing of their maturation in vivo) they produce the same effect in the host as endogenous IN, which is initiation of critical plasticity period
Capgras syndrome
-disorder in which a person holds a delusion that a friend, spouse, parent, or other close family member (or pet) has been replaced by an identical-looking impostor
-Ramachandran hypothesizes that the origin of the syndrome is a disconnection between the temporal cortex, and the limbic system, involved in emotions. More specifically, he emphasizes the disconnection between the amygdala and the inferotemporal cortex
Angular Gyrus
-right one has been associated with patio-visual attention
-plays a critical role in distinguishing left from right, by integrating conceptual understanding of the language
-also associated with orienting in 3D space, not because it interprets space but because it may control attention
In spinal cord _ organization of motor neurons
spatial- corresponds with location of muscles, different groups represented in different parts of spinal cord
_ horn are motor neurons
-move muscles that are proximal and distal in the corresponding part of the ventral horns
Skeletal muscles are made up of __
-Multiple fibers
-axons coming from motor neurons in ventral horn- spread and make NMJ which will innervate many muscle fibers
-one motor unit can innervate many muscles
NMJ is between _ and _
axonal terminal of motoneuron/ muscle fiber
Lower motor neuron
in spinal cord, final common pathway for initiation of movements
Upper motor neuron
in brainstem, cortex: voluntary movement initiation, planning, directing sequences of movement
Where are located motoneurons that innervate gastrocnemius muscle in the spinal cord?
in the ventral horns of lumbar segments
Motor unit
-one alpha-MN and all muscle fibers that innervates
-when one is activated it will innervate all of the muscle fibers that synapse with it in the NMJ
-single extrafusal muscle fiber is innervated by only one alpha-MN
-MN brings all muscle fibers that it innervates to threshold
Motor neuron pool
-all MN that innervate single muscle
-Axons innervating muscle fibers within the same muscles are near each other in spinal cord
-Location of axon groups distributed spatially related to muscle positions
-if you inject dye, you can label/map all motor units that correspond to muscle
-can be bigger of smaller depending on muscle and action on muscle
Axial muscles
-muscles for posture
-medial ventral horn
-many segments of the spinal cord
-communicate with each other and have bilateral projections
Limb muscles
-muscles for finer control
-lateral ventral horn
-fewer segments
-unilateral projections
Small alpha-MN (size principle)
-alpha-MN that stimulate few muscle fibers
-few fibers generate low force, have low threshold
-contract slowly
-fatigue resistant: red muscle fibers- rich in myoglobin and mitochondria
Larger alpha-MN (size principle)
-alpha-MN stimulate larger number of muscle fibers
-greater number of fibers can generate higher force
-pale muscle fibers: easily fatigued, sparse mitochondria, running, jumping
-generate large forces
-contract quickly
Three classes of motor units
1. S: slow, low force over long period of time
2. FR: fast, fatigue resistant, medium force over medium period of time
3. FF: fast fatiguable, high force over short period of time
How to increase force in muscles
-size principle recruitment
-activities like jumping and galloping have larger force than activities such as standing and walking
If all of none principle applies in a single muscle fiber how can you achieve more force in the muscles?
1. by recruiting more muscle fibers by single motor neuron
2. by recruiting more motor neurons
3. by recruiting more motor units
3 Ways to increase force
frequency modulation
1. recruitment
2. summation
3. tetanus
Number of motor units and their firing rate _ with voluntary force
Neural control of motor systems
command (efferent signal) -> output device (muscle/motor unit) -> output (muscle length)
Open loop control
-command is sent and it triggers an output
-open loop has no built-in correction
Feedback control
-monitor the output and make necessary changes in command to get desired result
-error between 'actual output' and 'desired output'
Stretch Reflex
-ex. of negative feedback loop
-Causes contraction of a skeletal muscle in response to stretching of the muscle.
-Monosynaptic reflex
-Patellar or knee-jerk (deep tendon,
myotatic) reflex: Stretching of a muscle →activation of muscle spindles →sensory neuron →spinal cord→motor neuron → muscle contraction
• Ipsilateral
Monosynaptic reflex arc
-only one connection between spinal cord neuron and muscle
-In between motor neurons and afferent fibers from periphery are interneurons
What controls contraction of muscle in response to stretch?
Muscle spindle- sensory specialization with its own muscle
Two types of sensory afferents
Group 1a (dynamic) and Group II (static)
Group Ia sensory afferent
-annulospinal: signal changes in length fire tonically in proportion to degree of stretch
Group II sensory afferent
-tonically active: steady state level of stretch and tension
-muscle tone
Muscle tone
steady level of tension in muscles
Reciprocal activation of antagonistic muscles
-adjustment in length of muscle
-supported elbow and pouring water shows this
Negative feedback
descending facilitation and inhibition -> alpha-MN -> muscle (force required to hold glass) -> disturbance (addition of liquid to glass) -> load -> length change in muscle fiber -> spindle receptor-> increases spindle afferent discharge-> back to alpha-MN
-innervates spindles (intrafusal muscle fibers)
-level of activity is named as gain (can be higher or lower and is constantly adjusted)
-co-activation with alpha
-innervated striated (extrafusal) muscle fibers
Gamma-MN gain
-degree to which the change in stretch effects the recruitment and resulting output of the alpha- motorneurons
-Under CNS control
-Contraction of the ends of the intrafusal fibers determines how much the afferents' endings are stretched
High gain
small stretch produces large effect
Low gain
small stretch produces small effect
Without gamma-alpha co-activation
-Stimulate alpha MN (stimulate etrafusal MN) → contraction of muscle
-If muscles are contracted but don't have gamma MN (activation of intrafusal MN)→ relaxation of muscle after a while
Gamma-alpha co-activation
-no decrease during muscle shortening
-When g-MN are activated these neurons cause intrafusal fiber contraction
-When dynamic g-MN fire, dynamic response of I a afferents is increased
-When static g-MN fire, static response of II afferents is increased
-During movement, postural adjustment
Golgi Tendon organ (GTO)
-between muscle fibers and tend
-measures muscle force
-lot of collagen fibers
-sensitive to change in muscle tension, but insensitive to passive stretch
-group Ib afferents
-control tension of muscle and reset to normal level
Tendon reflex
-Polysynaptic reflex
-Control muscle tension by causing muscle relaxation when muscle tension is great
-Sensory receptors- Golgi tendon organs
- ↑ Tension applied to the tendon → tendon organ stimulation → nerve impulse → spinal cord →motor neuron causes muscle relaxation and relieves tension
-negative feedback loop
-have to have local interneuron that results in inhibition
GTO and muscle force
-If output increases too much (I.e., force very large) this can trigger inhibition of the contracting muscle
-'Negative feedback' to control force
-Note the Ib afferent and inhibitory interneuron for flexor and the excitatory interneuron for extensor
Sequential contraction and relaxation of segments in leech
- locomotion isn't in spinal cord, regulated by higher centers (some brain stem)
Central pattern generator (CPG)
-organizes locomotion in spinal cord
-neural networks that produce rhythmic patterned outputs without sensory or central input
Locomotion in cat
-two phases: 1. stance/extension 2. swing/flexion and extension
-each limb has CPG that is responsible for alternating flexion and extension during movement
-make transection in spinal cord and movements are still permitted because of CPG allows for rhythmic movement
-if hind legs are paralyzed, put cat on treadmill and they will be able to walk
Lower motor lesions
-destruction of motor neurons in ventral horns of spinal cord
-result in flaccid paralysis of affected muscle
-ipsilateral damage
Flaccid paralysis
disease which is concerned with isolated degeneration of motor neurons in ventral horn of spinal cord, results in weak muscles, diminished reflexes, reduced muscle tone
Primary motor area (4)
-in precentral gyrus, anterior wall of central sulcus and anterior part of paracentral lobule
-has 6 horizontal layer
-afferents from other cortical areas and from ventrolateral posterior nucleus (VLp)
-efferents- pyramidal system
-commands and initiation of movement
Pyramidal system
30% from area 4, 30% from area 6, 40% from somatosensory area (1,2,3)
-Mostly contralateral representatation of skeletal muscles; muscles of axial skeleton and head ipsilaterally
-layer 5 in primary motor area is the largest pyramidal cells that ascend axons to subcortical regions and innervate different part of muscles: Stop in thalamus→ receives information from cortex, has ventral lateral nucleus
-All bundles go down and make pyramidal system
-Called pyramidal because pyramids are on ventral side of medulla, they are the corticospinal tract
-Come from cortex and cross in pyramids and go to the other side
-Pyramids are group of corticospinal tract
Premotor cortex
area 6 at lateral surface, planning of movement
Homunculus of primary motor area
-inverted representationof body, starting from below
-face is 1/3 of area 4
Supplementary motor area (6)
-located at medial surface of hemisphere
-lesion won't cause paralysis
Lesion on supplementary motor area
-akinetic mutism: no motivation for movements, recover after a few weeks
Betz cells
-giant cells in layer 5 of primate motor cortex
-Largest cells in the body- 100 um diameter
-Largest appear in primates
-Project to Spinal cord
-They are NOT the only corticospinal neurons
but appear responsible for fine movements of limbs
-axons make corticospinal tract
Pyramidal tract
1. corcticobulbar tract
2. corticospinal tract
Corticobulbar tract general
-project to brainstem nuclei (ex. facial and trigeminal motor nuclei)
-contralateral and bilateral pathways
Corticospinal tract general
-cross at pyramidal decussation (in medulla)
-major spinal projection along lateral spinal tracts and smaller projection along anterior medial tract (aka. ventral medial tract)
-upper and lower extremities, and trunk
Upper motor neuron lesion
-destruction of descending pathways
-lesions result in spastic paralysis
-occur in conditions affecting motor neurons in brain or spinal cord such as stroke, TBI, and cerebral palsy
-Babinski's sign
Spastic paralysis
-lesions in cortex, brain stem, or spinal cord
-stiff because they are losing descending projections from cortex that are excitatory and inhibitory (modulate movement), everything below lesion is damaged
Babinski's sign
- stroke bottom of foot, and toes fan out and dorsiflexion
-normal in babies because corticospinal tract hasn't developed fully yet
Facial nerve
-lower motor neuron
-paralysis of facial muscles because innervates upper and lower part of face
-ipsilateral loss of muscles
-Bell's palsy
Bell's palsy
-lower motor neuron disease caused by facial nerve
-floppy muscles on one side, hard to close eyes/blink or squint
Lesion in cortex or thalamus
-upper cortex disease
-lower part of face affected
-contralateral loss of muscles
Corticospinal tract
-internal capsule: bundle of axons that tract goes through
-midbrain: substantia nigra
-cross to other side at caudal part of pyramids in medulla
Reticulospinal tract
-upper motor neuros in brainstem
-postural and coordinated postural and limb movement
-tract that doesn't start in cortex but rather at brainstem
-control posture: 1. subject told to flex arms upon hearing tone 2. flexion of gastrocnemius precedes bicep flexion to compensate for change in weight distribution
-control involuntary movements
Lesion above crossing
contralateral side
Lesion below crossing
ipsipateral side
Upper motor neurons in brainstem descend _
Upper motor neurons in cerebral cortex descend _
Lower motor neurons in medial ventral horn descend_
ipsilaterally: axial and proximal limb muscles (posture and balance)
Lower motor neurons in medial ventral horn descend _
contralaterally: axial and proximal limb muscles
Lower motor neurons in lateral ventral horn descend _
contralaterally: distal limb muscles (skilled movements)
Upper motor neuron projections in monkey
1. Recording from cortical motor neurons in monkey
2. Put electrodes on arms and record EMG as result of activity of neurons
-Stimulate neurons in cortex and EMG
-EMG will summarize/average and will have response
3.Experiment showed that firing of cortical neurons change prior to movement
-Means that neurons trigger movement
-Found activity of different muscles in hand
-All muscles involved in flexion or extension of hand
-Control muscles group that all have the same goal
-Stimulate one part→ will have specific action
-Different from sensory system
4. result: firing of cortical neurons changed prior to movement -> cortical motoneurons control several lower motor neuron pools
Cortical stimulation in awake behaving animals initiates _
movement not activation of single muscles
Motor map
-new view of motor homunculus
-map of different coordinated directional movements or actions towards a goal not just activation of muscle groups
-Representation of cortical neurons in cortex
-Responsible for directional movement: Specific goals that cortical neurons regulate, Different groups of muscles but with same goal, Different orientation and organization of cortical neurons that have different movements
Activity of primary motor neurons is correlated with _ and _
Magnitude/ direction of force produced by muscles
Population code
-Activity of neurons that are tuned in different direction but as result of many of the neurons will have movement in specific direction
-Direction of movement is result of population of neurons in part of cortex that is responsible for those muscles
-Every movement is result of many neurons and their movement is averaged and you will have movement in that direction
Mirror neurons
fires both when an animal acts and when the animal observes the same action performed by another
adjusts accuracy and precision of motor behaviors
Basal ganglia
-initiates and suppress motor behaviors
1. Corpus striatum: striatum and pallidum
2. Subthalamic nucleus
3. Substantia nigra
-Facilitates cortical output that initiates and produces effective motor (emotional and cognitive) behaviors
- Inhibits cortical output that produces ineffective motor (emotional and cognitive) behaviors
-decision of which behaviors to be executed and given time
Lentiform nucleus
putamen and globus pallidus
-caudate nucleus, nucleus accumbens, putamen
globus pallidus: external and internal segments
How does that basal ganglia control movements?
provide control of motor behaviors mainly by receiving a copy of cellular excitatory activity from specific regions of the cerebral cortex (topographic) and then by influencing that activity in the same cortical region
Basal ganglia disorders
poor movement
extra movements
-cerebral cortex to caudate and putamen
-GPi & SNr to VA and VL of thalamus
-VA and VL to thalamus to cerebral cortex
Medium spiny neurons
-receive all input from Cortex & project to Globus Pallidus and Substantial Nigra Pars Reticulata
-activated before movement is performed: silenced in rest in striatum, not silenced in rest in pallidum
-Neurons in pallidum secrete inhibitory neurotransmitters
-They inhibit other targets
-They fire action potentials at steady high rate in the
absence of input
- Signals from striatum cause them to pause their inhibition-they operate using disinhibition principle.
-Globus pallidus internus (toward midline); GP externus-laterally
- The purpose of inhibition of cortical activity is to ensure that muscles rest when they are not in use to execute goal-directed motor behavior
Control of movement
-At rest, neurons in the striatum are quiescent, and in pallidum are
active, thereby inhibiting he thalamic excitation of the motor cortex
-Before and during initiation of movements, the striatum is active and inhibits pallidum, allowing excitation of the motor thalamic nuclei and send information to supplementary motor cortex and premotor cortex
-Corticospinal, corticoreticular and reticulospinal fibers modulate then motor neurons
-Diseases of basal ganglia result in unwanted movements
-depolarizes MSNs in direct pathway
- inc. cAMP
-in normal brain the dopamine through this receptor will excite the direct pathway and result in the excitation of the cortex
-dec. cAMP
-hyperpolarizes MSNs mostly in indirect pathway
-in normal brain will inhibit the indirect pathway and excite the cortex
Dopaminergic cells die and balance of indirect and direct pathways is disrupted in favor of indirect pathway (poor movements)
Parkinson's disease
-hypokinetic disease
-less dopamine leads to poor movement and dramatic tremor
-poor initiation of movement
-Dopamine can't cross BBB so use medicine eldopa (?) that is precursor of dopamine
-deep brain stimulation to help
Deep brain stimulation in Parkinson's patients
-inject canulodes that stimulate specific part of basal ganglia and modulate activity
-frequent target is sub thalamic nucleus (glutamate), want more glutamate and excitation and produce moment in patient
Huntington's disease
-striatum is damaged: degeneration causes part of indirect pathway to stop working- too much excitation
Ballism and Hemiballism
-Degeneration of the subthalamic nucleus and loss of influence of indirect pathway. Symptoms include involuntary violent, ballistic movements- extra movements
-modulate indirect pathway: loss of this in normal movement and will have extra movement which are violent and strong
Cerebellum functions
Main functions
1. To detect differences between indented and executed (actual) movement
2. And to reduce the error thought upper motor neuron
1. Movement: Coordination, correct time, force and synergy of muscle contractions
2. Posture
3. Eye movements
4. Some sensory and cognitive functions, e.g. Visual- spatial tasks
Cerebellum general
-Take up 10% of brain mass, but accounts 50% of neurons
-Cerebellar hemispheres control the same side of the body
-Structure: gray matter, white matter, four pairs of central nuclei
-Three cerebellar peduncles connect cerebellum with brain stem
-topographically organized
Women who doesn't have cerebellum
-dizziness and nausea
-problems walking steadily for most of her life, hadn't walked until she was 7
-speech only became understandable at the age of 6
-A new case of complete primary cerebellar agenesis: clinical and imaging findings
in a living patient
Cerebellar cortex regions
1. Cerebrocerebellum
2. Spinocerebellum
3. Vestibulocerebellum
Inferior cerebellar peduncle
-contralateral inferior olivary complex
-spinal cord, vestibular nerve and nuclei
Middle cerebellar peduncle
from contralateral pons
Superior cerebellar peduncle
-fibers from interposed and dentate nuclei to thalamus and motor cortex
-superior colliculus
Cerebellar inputs
I. frontal/ parietal cortex
A. Red nucleus
1. Inferior olive (crosses midline to cerebellar cortex/deep nuclei)
B. Pontine nuclei (crosses midline to cerebrallar cortex/ deep nuclei)
-spinal cord and vestibuli nuclei also go to cerebellar cortex/deep nuclei but don't have to cross midline
Cerebellar outputs
I. Cerebrocerebellum
A. dentate nucleus
1. Premotor cortex (motor planning)
II. Spinocerebellum
A. interposed and fastigial nuclei
1. motor cortex and brainstem (motor execution)
III. Vestibulocerebellum
A. Vestibular nuclei
1. lower motor neurons in spinal cord and brainstem (balance and vestibule-ocular)
control flow of information in cerebellar cortex
Granule cells
-control granule cell input to Purkinje cells
Stellate cells
-lateral inhibition of Purkinje cells
Cell types and Circuit
- Inputs: mossy fibers and climbing fibers
- Interneurons: granule cells, basket cells, Golgi cells, stellate cells
• Integration/Output - Purkinje cells
Convergence of Purkinje cells
-one cell make contacts with 200,000 parallel fibers
-one parallel fiber contacts many of these cells
-basket, stellate cells also converge on these cells
Mossy fibers
-originate in pontine nuclei, spinal cord, brainstem reticular formation, and vestibular nuclei
-excitatory projections onto cerebellar nuclei and granule cells
-large degree of divergence
-innervates hundreds of granule cells which send axons to cortical surface
Parallel fibers
-run parallel to the folds of the cerebellar cortex, where they make excitatory synapses with hundreds of Purkinje cells
Climbing fibers
-originate in inferior olive
-excitatory projections onto cerebellar nuclei and Purkinje cells
-each Purkinje cell receives a single input from one of these fibers
-each one of these cells makes about 10 connections with Purkinje cells
-restricted by extremely powerful input
Purkinje cells
-sole source of output fro cerebellar cortex
-inhibitory connections onto cerebellar nuclei (GABAergic inhibitory projections to deep cerebellar nuclei and vestibular nuclei)
-corrective signals from cerebellum consist of increases in discharge rate (due to reduced activity of these cells) or decreases in discharge rate (due to increased activity of these cells)
Vestibuloocular reflex
-When head moves, eyes move at the same speed to opposite direction to fixate an object
-Adaptation of eye movement is lost with cerebellar damage
-Exercise: spinning for a while and then sit and fixate on one spot- eyes will beat in direction of spinning
inability to standup and maintain direction of gaze
Midline lesions on cerebellum
-Could be caused by meduloblastoma during childhood
-In chronic alcoholism : adult ataxic gait (wide base walk, sways from side to side)
- Cerebellar nystagmus- interruption of connections of vermis with ocular motor nuclei, by way of vestibular nuclei and reticular formation
- Disturbance in equilibrium
Neocerebellar syndrome
-lesions of cerebellar hemispheres, central nuclei, superior cerebellar peduncles
-tremor at end of movement
-neocerebellar syndrome
-intermittent movements; lack of coordination of movements
-neocerebellar syndrome
-overshoot of pointing at object; opposite movements could not be performed
Cerebellar cognitive affective syndrome
result of posterior lesions of cerebellum- motor deficits and impairment in planning and reasoning of high skilled movements, such as playing of instruments or speech
Anterior cerebral artery
The frontal l.
-leg weakness
-Volunt. Leg movement - akinetic mutism
(severe; if both)
Middle cerebral artery
-Portion of frontal l. & lat surf. of temp./parietal l
-Most often occluded -areas of speech
Posterior cerebral artery
-Temp and occipital I
-thalamic syndrome
-color blindness
Basilar artery
supplies blood to brain stem
Vertebral artery
branches to spinal arteries and cerebrallar arteries
Cerebellar arteries
-AICA (anterior inferior cerebellar artery)
-PICA (posterior inferior cerebellar artery)
-SCA (superior cerebellar artery)
-Acute vascular event of the brain
-3rd leading cause of death in the US
- Primary cause of long-lasting disability
Types of stroke
1. Hemorrhagic
2. Ischemic
Hemorrhagic stroke
-result from many conditions that affect your blood vessels, including hypertension, overtreatment with anticoagulants and weak spots in your blood vessel walls (aneurysms)
-intracerebral hemisphere
-subarachnoid hemisphere
Ischemic stroke
-Thrombolic: clot formation in the location of the vessel blockage
- Embolic: vessel blockage by a clot, plaque or other obstacle that has travelled from somewhere else in the vasculature
-decreased blood flow
-tissue death: cerebral infarction
-penumbra: ischemic tissue potentially destined for infarction but not yet irreversibly injured and the target of acute therapies
Intracerebral hemorrhage
-Same symptoms as ischemic stroke
-15% of all strokes
-Least treatable and highest mortality -Typically occurs at small penetrating vessels
-Break in the blood brain barrier
Subarachnoid hemorrhage
-Rupture of an arterial aneurysm. These tend to form in or near the circle of Willis
-Blood flow into subarachnoid space
-5% of all strokes
-Sever headache vomiting and alertness decrease
Stroke symptoms
-Facial drooping: A section of the face, usually only on one side, that is drooping and hard to move
-Arm weakness: The inability to raise one's arm fully
-Speech difficulties: An inability or difficulty to understand or produce speech
-Time: If any of the symptoms above are showing, time is of the essence; call the emergency services or go to the hospital
Artery occlusion in anterior cerebral artery
-hemiparesis and somatosensory loss involving leg more than arm
Artery occulsion in middle cerebral artery
-Hemiparesis of face and arm more than legs; unilateral sensory loss, motor speech defect (Broca's aphasia - upper division);
-Comprehension of speech- Wernicke's Aphasia- lower division
Language areas affected by stroke
-Receptive language area (sensory language or posterior speech area) consists of auditory association cortex (Wernicke 's area 22, 30) in superior temporal gyrus
-Expressive speech area: Broca's area, motor speech area), area 44, 45
-Supplementary motor area on medial surface of the hemisphere is also necessary for normal speech
-Left hemisphere is dominant for speech: Planum temporale, region of the brain associated with language is larger in left than right hemisphere. 75% of people are right handed
Broca's area
-area 44,45
-language production: expressive aphasia
-favored hand: right hand people (>90% of left brain dominant) left hand people (80% right brain dominant)
-A cognitive disorder marked by an impaired ability to comprehend or express language in its written or spoken form
-This condition is caused by diseases which affect the language areas of the dominant hemisphere
-Clinical features are used to classify the various subtypes of this condition. General categories include receptive, expressive, and mixed forms of it
Wernickes area
-area 22, 30
-language understanding: receptive aphasia, also in dominant hemisphere
Conductive aphasia
lesions of the accurate fasiculus
Wernicke's aphasia
-Impairment in the comprehension of speech and meaning of words, both spoken and written, and of the meanings conveyed by their grammatical relationships in sentences
-caused by lesions that primarily affect this area, which lies in the posterior perisylvian region of the temporal lobe of the dominant hemisphere
Artery occlusion of posterior cerebral artery
-Alexia: inability to read
-isolated vision loss, or other sensory loss -Amnesia: if bilateral temporal
Stroke syndromes of telencephalon
-symptoms on contralateral side of lesion
-damage to internal capsule: primary symptom is loss of voluntary movement in contralateral arm/leg/lower face if corticospinal tract is involved
-middle cerebral artery
-posterior cerebral artery
-anterior cerebral artery
Middle cerebral artery stroke syndromes
1. Primary symptoms are contralateral
2. Weakness or paresis in opposite arm and lower face
3. Loss of sensation in opposite arm and lower face
4. Contralateral visual field loss due to optic radiations
5. Left sided lesions may involve Broca's or Wernicke's areas and result in aphasia
6. Loss Cognitive deficits related to prefrontal cortex
Posterior cerebral artery stroke syndromes
1. loss of contralateral visual field
2. agnosia due to damage to inferior temporal lobe
Anterior cerebral artery stroke syndromes
1. Primary symptom is loss of sensation and movement in lower limb due to damage to the sensory‐motor strip on the medial surface
2. Possible affective issues due to cingulate cortex or medial prefrontal cortex
Immediate ischemic stroke treatment
-tPA: Tissue plasminogen activator-thrombolytic
-Best if given within 3 hours of stroke. Improves outcome post stroke by 25%
-But risk of intracerebral hemorrhage
-Physical extraction of the clot by arterial catheter
Ischemic stroke treatment if developed
-Cell death blockers, excitotoxicity blockers, anti- inflammatory
-Transcranial laser therapy
Post stroke therapies
1. physical therapies: mirror box, intensive physical and speech therapy, occupational therapy
2. Emerging rehab therapies: Constraint-induced Movement Therapy (CIMT) and Transcranial Magnetic Stimulation (TMS)`
3 layers in cerebellar cortex
1. molecular
2. Purkinje- output cells, send information from cerebellar cortex to CNS
3. granular
Which fibers ______________ are the output of the cerebellar .
'cortical inhibitory loop.'
Purkinje cells
Purkinje cells ____________ their targets in the deep cerebellar nuclei.
The gait disturbances associated with cerebellar ataxia can be distinguished from ataxia associated with parkinsonisms by
Cerebellar ataxia is characterized by wide steps while parkinsonian gait is characterized by small shuffling steps
Which best describes the laterality of effects of cerebellar lesions?
impaired movements ipsilateral to the lesion- b/c they are double crossed pathways