Ch. 4 Study Guide Neuro.pdf

4.1 Cerebellum Cerebellum considered to be the “little brain” -is located in the posterior inferior aspect of the cranium -collaborates with the vestibular system and proprioceptive input from the SC, the cerebellum serves to integrate the incoming sensory information to and from, quality of movemen...

4.1 Cerebellum Cerebellum considered to be the “little brain” -is located in the posterior inferior aspect of the cranium -collaborates with the vestibular system and proprioceptive input from the SC, the cerebellum serves to integrate the incoming sensory information to and from, quality of movement receives information from the cerebral cortex through the pontine nuclei regarding intended movements or what the brain wants to do V Is then able to coordinate movements by comparing the A 2 3 intended movements of the cerebral cortex to new movements that actually occur via sensory feedback ~ Then adjust the quality and amplitude of the movement -this all happens non-consciously to prove smooth, accurate movements throughout the body for overall balance, posture and coordination 3 cortical layers in cerebellum (all gray matter) -cerebellum’s gray matter is found in the outer layer and the white matter is found inferior to that Outer layer- Molecular Layer contains interneurons such as stellate cells, basket cells and granule cells Middle Layer-Purkinje Cell Layer contains purkinje neuronal cell bodies -cells convey all cerebellar’s output signals and are the largest in the brain -provides inhibitory signals to the cerebellum and vestibule nuclei -purkinje cells are oriented such as they fend outwards, upwards and posteriorly Granule Cell Layer consists of interneurons that send signals to purkinje fibers -send signals into the molecular layer forming these parallel red fibers at the molecular level -signals run perpendicular to the dendritic fan like fibers of the purkinje cells White Matter formed by 1. Climbing and 2. Mossy fibers -both fibers carry excitatory signals into the cerebellum -mossy fibers Originates from pontine nuclei derive from the brain stem, SC and cerebral cortex and convey somatosensory, arousal, balance, posture and intended movement signals to the granule cells -climbing fibers - from the inferior olivary nucleus in the medulla oblongata carries signals on motor errors to improve the timing their signals have significant influence on purkinje cell activation Cerebellum (Lying inferior to occipital lobe) Split into 2 hemispheres Each hemisphere is further separated into 3 lobes: 1. Anterior lobe 2. Posterior lobe 3. Flucculonodular lobe Cerebellum can be split by its fxnal divisions First includes: midline vermi— separated the two cerebellar’s hemispheres and the paravermi which is part of the cerebellar hemispheres but adjacent to the vermis itself Second includes: lateral hemisphereslateral to the paravermi Third would be: the follicular modular lobe -connection from the cerebellum to the rest of the CNS occurs in the cerebellar peduncles There are 3: superior, middle and inferior cerebellar peduncles can be seen in the posterior aspect of the brain stem and contain or consist of axons Superior cerebellar Peduncles connects to the midbrain and mainly contains efferent signals that arise in the cerebellum and project towards the cerebral cortex -carry some efferent signaling from the SC via the anterior spinal cerebellar tracts Middle cerebellar peduncle carries only afferent axons from the cerebellum to pontine nuclei/superior colliculus Inferior peduncle carries both efferent and afferent signals, coordinating signals from the SC, vestibular system and inferior olivary nucleus (goes to medulla) -efferent signals out to the vestibular nuclei and the reticular formation Midline structures form the spinocerebellum mainly coordinates gross limb movements Vestibulocerebellum focuses on balance, equilibrium, and coordinated eye movements Cerebrocerebellum fxns in the lateral hemispheres of the cerebellum with input from the cortex coordinating precise distal extremity movements Summary: -the gross anatomical structure of the cerebellum has 3 layers, three lobes and three peduncles, each with its own distinct cell types, or roles and function -functionally the cerebellum can be divided into 3 roles based on the lateral, central and lower regions to coordinate movement in the trunk, head and limbs spino cerebellum w/ 4 tracts (gross limb movement) 4.2 Cerebellum Tracts vestibular cerebellum receives input from IPSI vestibular apparatus via vestibular nuclei sends signals back to IPSI vestibular nuclei coordinates eye movement, muscles related to balance & equilibrium cerebral cerebellum receives signals from and sends signals out to cerebral cortex modifies signals in cortical spinal, critical brain stem, & rubospinal tracts signals from cerebral enter via pontine nuclei through middle cerebellum peduncles & exit via deep cerebellum nuclei & dentate nucleus motor planning, timing and cognitive functions (language, comprehension, goal directed behavior & spatial function) deep cerebellar nuclei involved in spinocerebellar pathways HIGH FIDELITY; posterior spinocerebellar & cuneocerebellar (proprioceptive info to IPSI cerebellar hemisphere from body) posterior spinocerebellar pathway : proprioceptive signals from lower trunk / limbs info from nucleus dorsal is through inferior cerebellar peduncles terminates in cerebellar cortex cuneocerebellar carries proprioceptive info from IPSI upper trunk, upper limb, neck to lat cuneate nucleus & through inferior cerebellar peduncle terminates in cerebellar cortex anterior spinocerebellar & rostrospinocerebellar: info on internal feedback on proprioceptive input from SC • activity of spinal reflexes & descending motor commands anterior spinocerebellar: originates in thoracolumbar area & only area w/ decussation ↓ input to both cerebellar hemispheres via superior cerebellar peduncles ↓ help w/ intralimb LL coordination (walking) rostrospinocerebellar & signals from UL and trunk to IPSI cerebellum via superior & inferior cerebellar peduncles Vestibulocerebellar EFFERENT pathway ↑ output from flocculonodular lobe ↓ impacts eye movement, ↓ coordinates motor output from vestibular nuclei down into lat/med vestibular tracts for balance & posture cerebrocerebellar: in lat cerebellar hemisphere S converges on dentate nucleus ↓ projects to CL thalamus & red nucleus d signals relayed to cerebral cortex CL to cerebral hemisphere that sent them cerebellum modifies activity in IPSE lat cortical spinal & rubospinal tracts spinocerebellar: originate in paravermi & vermi indirect impact on medial motor tracts (all 4 in pic) • medial corticospinal tract: IPSI • 3 others CL to cerebral cortex INDIRECT connection: signals from vermi/paravermi thalamus brain stem nuclei & 2 deep cerebellar nuclei (fastigiado nucleus & interposed nuclei) Then goes to the 4 tracts Summary: • cerebellum = powerhouse of neural signals, modify fxn based on sensory info. Different than cerebral hemispheres bc receives signals from and sends signals to IPSI body • vestibular cerebellum = coordinate balance, posture, eye mvmts • spinocerebellum: coordinates medial motor tracts • cerebrocerebellum: coordinates lateral motor tracts what is inhibition: preventing the pathway from moving forward disinhibition: inhibiting the inhibitor 4.3 Cerebellum Dysfunctions Gait Ataxia patient has difficulty narrowing the station and maintaining balance -typically will have a wide stance to try to maintain balance -often time have unsteadiness in the trunk -there could be some truncated titubation (oscillation while standing) which is anterior posterior to have a tremor at about 3 hertz -also a tendency to lunge or jerk sideways and the patient has to catch themselves -one of the ways to bring out this particular type of problem is to narrow the station, asking the patient to walk tandem Gait Ataxia uncoordinated movement of the legs leading towards poor balance Things to look out for: varied steps in length poor lateral weight shift forward momentum which characterizes the staggering gait pattern -cerebellar lesions impacting the vestibular cerebellum could create nystagmus of the eyes Nystagmus is an involuntary rhythmic shaking or beating of the eyes often seen in those with vestibular problems -nystagmus can be classified as a horizontal and verticals recto on or could be rotators based on the direction of the rhythmic beating Dysarthia describes incoordination of the muscles producing speech surrounding the vocal cords and is often seen with problems arising in the cerebrocerebellum -muscles are coordinated symmetrically with timing for close and opening to produce clear articulate speech -in cerebellar lesion, this is likely to be impacted creating slurred speech, low tonal speech, altered air passage and other speech production deficits -individuals with cerebral cerebellar issues may also present with ataxia in the fingers such as with finger opposition Dysdiadochokinesia describes the inability for someone to produce rapid alternating movements such as supination and pronation of forearm or tapping one’s toes Dysmetria inability to accurately move a specified distance -typically see this in a finger to nose or finger to target test where the individual often misses the target typically moving too far- - knows as overshooting Action tremor is a rapid alternating contraction of the antagonist and agonist muscle surrounding a joint during movements -due to poor timing of muscle activity -results in the shaking of a limb as it attempts to move- - not seen while at rest -can result from a spinal cerebellar impairment -people with action tremor will attempt to control this by limiting the movement at one joint or what we call movement decomposition Somatosensory ataxia also leads to uncoordinated movement but that is actually due to limited somatosensory feedback from the limbs and trunk reaching the cerebellum to coordinate the motor signals Cerebellar ataxia vs Somatosensory ataxia L Evaluation of coordination and balance test with eyes OPEN which provides visual sensory feedback ↓ Eyes CLOSED Performance is worse w eyes closed then proprioceptive feedback to the cerebellum is insufficient to coordinate signals Summary: Damage to the cerebellum impacts its ability to coordinate somatosensory information to modulate motor response results in various impairments such as 1. gait ataxia 2. dysmetria 3. dysdiadichokinesia 4. nystagmus 5. dysarthria 6. action tremor 4.4 Basal Ganglia: Overview Basal Ganglia location • near base of cerebral hemisphere, ant/inf to thalamus What are basal ganglia? • group of nuclei/gray matter • work w/ cerebellum to turn on/off motor activity in vertical motor tracts • made of 5 structures caudate (makes C structure around other basal ganglia) make up striatum in putamen ventral striatum globos pallidus has an externus/internus part (lentiform nucleus) subthalamic nucleus in midbrain w/ substantia nigra substantial nigra contains melanin Lentiform nucleus: made of putamen & globus pallidus • separated from thalamus by internal capsule neurotransmitters involved in incoming signals to basal ganglia • glutamate • acetylcholine • serotonin excitatory inhibitory inside basal ganglia • glutamate • GABA • dopamine from substantia nigra efferent signaling • controlled by GABA • inhibits thalamus, pons, & reticular formation all mediate neural activity * activation via basal ganglia requires disinhibition 7 loop circuits basal ganglia are involved with • decision making • judgement • emotions • learning • eye movements • motor output non motor loops • goal-directed: info for making decisions, planning, choosing a motor plan head of caudate & globus pallidus -> send info to ventral anterior thalamic nuclei • social behavior: self control & prioritizes info ventral prefrontal cortex -> head of caudate & substantia nigra ->medial dorsal thalamic nuclei • emotion loops: emotion, motivation & reward seeking behavior, cognition, & motor systems facial expressions (masked individuals w/ deficits in this region of the brain from medial prefrontal cortex -> ventral striatum & pallidum of globus pallidus internus -> medial dorsal thalamic nuclei pure motor loops • hyperdirect • go/direct • no go/ indirect • oculomotor for eye movement summary: basal ganglia & cerebellum work together to modulate descending motor control by choosing appropriate motor plans. also involved in non motor functions like goal directed behavior, emotion & motivation, & social behavior w/ projections to & from prefrontal cortex 4.5 Basal Ganglia: Overview Ocular Motor Loop of BG responsible for directing attention to a space and for eye movements, particularly fast eyes movements, such as saccades, so that one can direct gaze to a prioritized target -links the frontal and supplementary eye fields of the cortex, the caudate body and the substantia nigra and then the ventral anterior thalamic nuclei BG Motor Loop: the Players -frontal cortex: motor and premotor cortex -ventral lateral and ventral anterior thalamic nuclei and caudate nucleus, putamen, globus pallidus internal and external -subthalamic nuclei and substantia nigra within the mid brain, both the substantia nigra pars compacts and substantia nigra pars reticulata Less voluntary movement BG: Disinhibition fxns based on the concepts of disinhibition -essentially means that motor circuitry is generally inhibited or chained down -role of BG would be to activate the circuitry by disinhibition or removing “ball and chain” PATHWAYS Hyperdirect Pathway leads to significant inhibition of the cerebral cortex, therefore inhibition of voluntary movement cortex -contain excitatory signal from the cerebral cortex to the subthalamis nucleus -increases inhibition of the motor thalamus by globus pallidus -the motor thalamus then is less able to excite the cortex, decreasing voluntary movement -the cerebral cortex is trying to signal a new motor program or voluntary movement, the hyperdirect pathway inhibits any ongoing previous motor programs -one the hyper direct pathway is able to stop any ongoing motor programs, the remaining two pathways go into effect ⭐ Direct- Go Pathway facilitates disinhibition of the motor thalamus, effectively signaling “go”, or allowing activation of the frontal cortex of a specific voluntary movement In the direct pathway -the cerebral cortex activates or excited the caudate and the putmamen -this transient activation is then able to inhibit the globus pallidus inter us. w inhibition of the globus pallidus, the inhibition of the thalamus is lessened therefore, increasing activation or transient activation of the frontal Indirect- No-Go Pathway begins in the caudate putamen, and involves the inhibition of the globus pallidus externus -these inhibitory signals decrease the tonic inhibition of the subthalamic nucleus -w this disinhibition, the subthalamic nucleus is able to send more excitatory signals to the globus pallidus internus, which then is able to increasee its inhibition of the thalamus -The thalamus, now further inhibited, decreases excitatory signals to the frontal cortex suppressing motor programs Combined these 3 motor loops of hyperdirect, direct and indirect pathways work together to coordinate the seamless switch bw motor plants Note: The BG have impact on the activities in areas extending beyond voluntary movements via the lateral cortical spinal and reticulospinal tracts -it also controls postural and girdle muscle activity via direct communication with the peduncle pontine nucleus and walking patterns via the midbrain locomotor regions Both require signals to the reticulospinal tracts hyperdirect goes directly to STN and indirect/direct start w/ striatum 4.6 Basal Ganglia: Dysfunctions hypokinetic problems: lil disinhibition of thalamus, lil activation of GO pathway & excessive activation of NO GO ex: parkinson’s , insufficient movement/motor activation hyperkinetic problems: too much disinhibition of thalamus by excessive activation of GO pathway or lil activation of NO GO ex: dystonia, huntingtons disease Dopamine in relation to Basal Ganglia • neurotransmitter • used by substantia nigra & striatum to mediate signals from caudate & putamen to other basal ganglia Parkinson’s • less dopamine available b/c neuronal degeneration in substantia nigra compacta & peduncle pontine nucleus direct pathway • lack of dopamine -> decreased ability of caudate & putamen to inhibit globus pallidus -> inhibition of thalamus & decreased activation of frontal cortex indirect pathway • lower dopamine availability -> increased inhibition of globus pallidus -> increased facilitation of globus pallidus & more inhibition of movement overall: hypokinesia= too much inhibition, too little dopamine hyperkinesia: too little caudate/putamen, too much movement (decreased amplitude of movement) neuron degeneration decreases signaling in • indirect pathway caudate & putamen less able to inhibit globus • pallidus external segment globus pallidus inhibits subthalamic nucleus • -> decrease activity in globus pallidus internal segment increased inhibition of thalamus -> increased • excitability of frontal cortex characteristics • decreased amplitude of movement • cogwheel rigidity (stretching a muscle feels like a ratchet where increased resistance come off & on throughout Akinesia: lack of movement bradykinesia: slowed movement • rapid alternating movements become progressively slower w/ small amplitude cog wheel rigidity: on & off resistance when stretching a muscle lead-pipe: constant level of resistance throughout ROM spasticity: velocity dependent resistance (may not be present when slow but present when fast stretch) Resting tremor: alternate involuntary contraction of agonist/antagonist muscle • normally limb @ rest & disappears w/ voluntary movement intention tremor: tremor seen during movement not at rest postural unsteadiness • parkinson’s or similar • lack of appropriate righting rxns & relative whole body rigidity ex: if have kyphotic posture & lose balance posterior may fall like tree gait w/ parkinson’s • decrease step length • foot clearance • forward kyphotic posture • freezing bc of inability to motor plan ex: trying to turn around the cone overall parkinson’s: voluntary motor plans initiated through basal ganglia impaired bc lack of dopamine • need external cues ex: visual, tactile, audio to enhance cortical signaling in hyper direct loop to increase subthalamic nucleus to increase voluntary movement more symptoms related to parkinsons micrographia: amplitude or size of letter/ movements used to write letter decrease over time hypomia: mask face appearance • no conscious emotional loop through basal ganglia impaired • can’t naturally present emotions through facials hypophonia: low amplitude of speech production dystonia: sustained involuntary muscle contraction (localized or distal) ex: writer cramp, neck torticollis, whole body during walking twisting movements • choreiform gait: constant involuntary jerky rapid movements • disinhibition of thalamus & constant excitation of motor cortical areas ex: can have oral facial dyskinesias • heavy movement on one side or grimace • some purposeful movements but then it will slowly go summary: dopamine from substantia nigra facilitates disinhibition in direct/indirect pathways, involved in parkinson’s damaged basal ganglia = impacts ability to calibrate or initiate movement or muscle activation leading to hypokinesia or hyperkinesia