CH2-Neurobases of Motor Speech & Its Disorders Flashcards
1
Q
Major Anatomic Levels of the Nervous System
A
- Supratentorial Level
- Posterior Fossa
- Spinal
- Peripheral
2
Q
Supratentorial
Anatomic, Skeleton, Meninges
A
- located above tentorium cerebelli, lateral to falx cerebri
- Skull - anterior and middle fossa
- Meninges-horizontal membrane forms upper border of posterior fossa,covers upper surface of cerebellum and separates anterior and middle fossae from posterior fossa
- Includes :
- paired frontal
- temporal
- parietal
- occipital lobes
- basal ganglia
- thalamus
- hypothalamus
- cranial nerves I (olfactory)
- cranial nerve II (optic)
3
Q
Supratentorial
Ventricular
System
A
- lateral & third ventricles
- Subarachnoid space
4
Q
Supratentorial
Vascular
System
A
- Carotid arterial system
- Opthalmic arteries
- Middle Cerebral Arteries
- Anterior Cerebral Arteries
- Vertebrobasilar system
- Posterior Cerebral Arteries
5
Q
Supratentorial
Motor Speech Disorders
A
- Apraxia of speech
- Dysarthrias
- Spastic
- Unilateral
- UMN
- Hypokinetic
- Hyperkinetic
6
Q
Posterior Fossa
Anatomic, Skeleton,
& Meninges
A
- Anatomic - Brainstem (pons, medulla, midbrain, and cerebellum)
- origin of cranial nerves III - XII (oculomotor, Trochlear, Trigeminal, Abducens, Facial, Cochleovestibular, Glossopharyngeal, Vagus, Accessory, Hypoglossal
- several represent the last neural link or final common pathway (FCP)
- Cranial nerves serving speech are part of PNS - crucial to understanding flassic dysarthria with stems from PNS, not CNS dysfunction like all other types.
- origin of cranial nerves III - XII (oculomotor, Trochlear, Trigeminal, Abducens, Facial, Cochleovestibular, Glossopharyngeal, Vagus, Accessory, Hypoglossal
- Meninges - Below Tentorium Cerebelli
7
Q
Posterior Fossa
Ventricular System
A
- Fourth Ventricle
- Subarachnoid Space
8
Q
Posterior Fossa
Vascular System
A
- Vertebrobasilar system
- vertebral arteries
- basilar artery
9
Q
Posterior Fossa
Motor Speech
Disorders
A
- Dysarthrias
- spastic
- unilateral upper motor neuron
- hyperkinetic
- ataxic
- flaccid
10
Q
Spinal
Anatomic, Skeleton & Meninges
A
- Skeleton - Vertebral Column
- begins at foramen magnum, large opening in posterior fossa
- surrounded by bony vertebral column
- 7 cervical, 12 thoracic, 5 lumbar vertebrae
- 31 pairs of spinal nerves (attached by dorsal and ventral nerve roots)
- Meninges - Spinal Meninges
11
Q
Dorsal
Roots
A
Dorsal = posterior
Posterior nerve roots that are sensory in function
12
Q
Ventral
Nerve Roots
A
- Ventral - anterior
- Ventral nerve roots are motor in function.
13
Q
Peripheral
anatomic, skeleton
& meninges
A
- Anatomic- cranial and spinal nerves
- most of cranial nerves originate in the brainstem, exit through skull and travel to muscle destinations.
- spinal nerves contain joined dorsal and ventral roots, enter peripheral level as they emerge from the vertebral column to travel to their muscle destinations.
- Skeleton -
- Face and skull
- Noncranial & nonspinal bones
- Meninges - none
14
Q
Peripheral
Ventricular
System
A
None!!
15
Q
Peripheral
Vascular System
A
- Branches of major extremity vessels
16
Q
Peripheral
Motor Speech Disorders
A
Dysarthria:
- Flaccid
17
Q
Major Functional
Longitudinal Systems
A
- neurological diagnosis begins with linking clinical signs and symptoms to one or more of major longitudinal systems of nervous system.
- Systems contain groups of structures with specific functions
- called longitudinal = activities of the system are evident over the length of nervous system (from supratentorial to the peripheral level)
- Internal Regulation System (Visceral System)
- Cerebrospinal Fluid Sstem (Ventricular System)
- Vascular System
- Consciousness System
- Sensory system
- Motor system
18
Q
Internal Regulation System
(Visceral System)
A
- represented at all major anatomic levels of nervous system.
- Includes
- hypothalamus
- parts of limbic lobe supratentorially
- reticular formation
- portions of some cranial nerves in posterior fossa
- longitudinal pathways in brainstem & spinal cord
- ganglia
- receptors & effectors at periphery.
- contains afferent & efferent components that interact to maintain homeostasis through regulation of visceral glands and organs.
19
Q
Cerebrospinal Fluid System
(Ventricular System)
A
- Comprised of:
- ventricular system and subarachnoid space
- Ventricular system - in depths of brain
- ventricles - cavities that contain CSF, produced by choroid plexuses in each ventricle.
- CSF- circulates through ventricles & subarachnoid space and absorbed by arachnoid villi in brain or leptomeninges in spinal cord subarachnoid space.
20
Q
Cerebrospinal Fluid (CSF)
function & location
A
- Function - to cushion the CNS against physical trauma
- help maintain a stable environment for neural activity.
- Location -
- supratentorial
- posterior fossa
- spinal levels
21
Q
Vascular System
A
- lifeblood of nervous system
- found within all major anatomic levels
- provides oxygen and other nutrients to neural structures and removes metablic waste from them.
- Major locus of abnormalities that can lead to MSDs.
- blood vessels that supply brainstem and cerebral hemispheres arise from aortic arch in chest.
- Bloodenters brain through:
- Carotid system
- Vertebrobasilar system
- two systems communicate with each other through channels in brainstem (Circle of Willis)
22
Q
Vascular disturbances
in
Vascular System
A
Vascular disturbances :
L or R carotid artery = Dysarthrias
L or R anterior and middle cerebral arteries = Dysarthrias
L middle cerebral artery = common cause of apraxia of speech and aphasia
vertebrobasilar system = often leads to MSDs
23
Q
Consciousness
System
A
- crucial to maintaining wakefulness, consciousness, awareness of environment, selective & sustained attention
- Malfunctions - contribute to cognitive deficits
- in language & communication
- indirectly affect motor functions, including speech
- structures- found only at supratentorial and posterior fossa levels
- includes:
- reticular formation
- ascending projection pathways
- portions of thalamus
- pathways to widespread areas of cerebral cortex
- portions of all lobes of cerebral cortex
- includes:
24
Q
Sensory
System
A
- Found in all major anatomic levels of the nervous system
- includes:
- peripheral receptor organs
- afferent fibers in cranial, spinal and peripheral nerves
- dorsal root ganglia (spinal level)
- ascending pathways in spinal cord and brain stem
- portions of thalamus
- thalamocortical connections
- sensory cortex in temporal, parietal, and occipital lobes
- includes:
- special sensory systems such as hearing and vision, are also located at peripheral, posterior fossa, and supratentorial levels
25
Q
The Motor System
A
- present at all major anatomic levels of nervous system
- directly responsible for all motor activity involving striated muscle
- Includes:
- efferent connections of cortex, esp. frontal lobes
- basal ganglia
- cerebellum
- related CNS pathways
- descending pathways to motor nuclei of cranial and spinal nerves
- efferent fibers within cranial and spinal nerves
- striated muscle
- Essential to : normal reflexes
- maintaining normal muscle tone & posture
- planning, control and executions of voluntary movement (incl. speech)
- Lesions in nonmotor areas of nervous system can produce alterations in speech by indirect effects on motor system.
26
Q
Localizing Nervous System Disease &
Determining Its Course
A
- neurologic signs and symptoms generally reflect the location of a lesion, not necessarily its specific cause.
- Disease can be localized on the basis of history and clinical examination.
- Broad Categories for describing localization & history of disease
- Localization
- Focal
- Multifocal
- Diffuse
- Development
- Acute
- Subacute
- Chronic
- Evolution
- Transient
- Improving
- Progressive
- Exacerbating-remitting
- Stationary (or chronic)
27
Q
Categories for Localization
of
Neurologic Disease
A
- Focal - involving a single circumscribed area or contiguous group of structures
- Multifocal- involving more than one area or more than one groupof continguous structures (e.g. cerebellar and cerebral hemisphere plaques associted with MS)
- Diffuse - involving roughly symmetric portions of the nervous system bilaterally (e.g. generalized cerebral atrophy)
28
Q
Development of
symptoms of disease
A
- Acute - within minutes
- Subacute - within days
- Chronic - within months
29
Q
Evolution (Course) of the disease
A
Evolotion or course of disease after symptoms have developed can be:
- transient - when symptoms resolve completely after onset
- improving - severity is reduced but symptoms are not resolved
- Progressive - symptoms continue to progress or new symptoms appear
- Exacerbating-remitting - symptoms develop, then resolve or improve, then recur and worsen, and so on
- Stationary (or chronic) - symptoms remain unchanged for an extended time
30
Q
Broad Etiologic
Categories
A
Each category can produce MSDs, but distriution of MSD types varies across causes.
- Degenerative Diseases- characterized by gradual decline in neurologic function of unknown cause.
- Inflammatory Diseases - include but not limited to infectious processes; inflammatory response to microorganisms, toxic chemicals, or immunologic reactions
- Toxic-Metabolic Diseases - vitamin deficiencies, thyroid hormone deficiency, genetic biochemical disorders, complications of kidney and liver disease, hypoxia, hypoglycemia, hyponatremia, and drug toxicity which alters neuronal function.
- Neoplastic Diseases - caused by rare cell division of neurons; astrocytomas (tumors), cancer
- Trauma- traumatic injury from precipitating event (auto accident, fall, gunshot wound, etc.)
- Vascular Diseases- most common cause of neurologic deficits and MSDs (e.g. stroke/CVA = neurons are deprived of oxygen and glucose due to interruption of blood supply)
31
Q
Degenerative
Diseases
A
- L - Diffuse; Focal
- D- Chronic
- E- Progressive
- Characteristics-
- gradual decline in neurologic function of unknown cause
- neurons atrophy & disappear or specific neuronal changes occur (neurofibrillary tangles in Alzheimer’s disease)
- genetically determined that share basic mechanisms that lead to neuronal death
- differences reflect localization of affected neurons and order and pace of degeneration.
- most often chronic, progressive, and diffuse, sometimes begin with focal manifestations
- cause found then shifted to specific disease category
32
Q
Inflammatory
Diseases
A
- L- Diffuse, focal
- D- Subacute
- E- Progressive; Exacerbate or remit
- Characteristics- include but not limited to infectious processes
- inflammatory response to microorganisms, toxic chemicals or immunologic reactions
- hallmark - outpouring of white blood cells
- many located in leptomeninges & CSF (meningitis) or brain parenchyma (encephalitis)
- inflammation in PNS can occur in single nerves (mononeuritis) or multiple (polyneuritis).
- some are focal - may have abscess formation, leaving a cavity that shows loss of enclosed brain tissue –> exerts mass effects on nearby structures.
33
Q
Toxic-Metabolic
Diseases
A
- L- Diffuse
- D- Acute, Subacute, Chronic
- E- Progressive, Stationary
- Characteristics- due to metabolic conditions that alter neuronal activity ( vitamin deficiencies, thyroid hormone deficiency, kidney/liver disease, hypoglycemia, etc.)
34
Q
Neoplastic Diseases
A
- L- Focal
- D- Chronic, Subacute
- E- Progressive
- Characteristics - due to neurons undergoing cell division creating neuronal neoplasms (neurocytomas); rare
- astrocytes - reactive
- astrocytomas - most common primary CNS tumor
- tumors named after cell types from which they arise (leptomeninges = meningiomas; Schwann cells = schwannomas)
- Primary nervous system tumors rarely metastasize (spread) outside CNS; but systemic cancer can spread to CNS
- Tumors create focal signs and symptoms; chronic/progressive in course
- not all progressiv emass lesions are neoplasms (hematomas and edema are nonneoplastic)
35
Q
Traumatic
Injury
A
- L- Diffuse, Multifocal, Focal, Acute
- D- Acute
- E- Improving, Stationary
- Characteristics - often diffuse initially (concussion) with course of improvement or resolution
- residual focal signs and symptoms reflect areas of severe anatomic damage
- exception to acute onset of signs & symptoms: can occur in subdural hematoma–> bleeding is under low pressure cause of location in veins crossing from brain to dural sinuses where blood is dreained from brain; blood accumulates slowly, and symptoms may not emerge for days or longer.
- TBI- subdivisions : Penetrating & Closed Head Injury (CHI)
- Penetrating - head wounds (bullets, shrapnel) = focal neurologic abnormalities
- CHI = diffuse abnormalities
36
Q
Penetrating
TBI
A
- penetrating head wounds (e.g. bullets, shrapnel)
- produces focal neurologic abnormalities
- can be combined with CHI
37
Q
Closed Head Injury
(CHI)
A
- type of TBI associated with diffuse abnormalities
- major causes - vehicle accidencts, falls, sports injuries
- Common deficits - Cognitive, Neurologic & motor impairments
- up to 60% may be dysarthric
- Injuries from CHI can create focal lesions, diffuse axonal injry and super impose hypoxia or ischemia and microvascular damage
- coup injuries & contrecoup lesions
- diffuse axonal injury contributes to neuro deficits in CHI (mild-severe)
38
Q
Coup injuries & Contrecoup lesions
A
coup injuries- focal contusions (superficial injuries characterized by leptomeningeal hemorrage and edema) often occur at site of impact and result in focal neurologic deficits
contrecoup lesion - injury associated with acceleration; motion of brain can cause trauma at sites opposite point of impact causing lesion
most common sites orbitofrontal region & anterior temporal lobes; where brain abuts on edges of skull
39
Q
Diffuse axonal injury
A
- effect of trauma
- contributes to neurologic deficits in mild-severe CHI
- occurs more frequently when trauma is associated with rotational forces
- reflects shearing of axons in numerous brain areas
- generates physiologic response in affected axons
- leads to swelling and Wallerian degeneration=disrupting functions of networks
40
Q
Vascular
Diseases
A
- L- focal, multifocal, diffuse
- D- Acute
- E - Improving, Stationary, Transient, Progressive
- Characteristics -
- most common cause of neurologic deficits & possibly MSDs.
- most common cerebrovascular disease = stroke (aka infarct & CVA) => ischemia
*
41
Q
Ischemia
A
neurons deprived of oxygen and glucose because of interruption in blood supply (ischemia) due to stroke/CVA
- common cause = embolism
- other causes = thrombosis- narrowing and occlusion of artery at fixed point
42
Q
Thrombosis
A
- narrowing and occlusion of an artery at a fixed point
- also causes ischemia
- reflects buildup of atherosclerotic plaque
- usually occurs in the internal carotid, vertebral or basilar arteries
- somestimes preceded by transient ischemic attacks (TIAS).
- other sources of thrombotic strokes- spontaneous or traumatically induced dissections of the carotid, vertebral, or intracranial arteries
- mass effects on arteries by turmes, or aneurysms
43
Q
Transient Ischemic Attacks
(TIAs)
A
- characterized by neurologic symptoms that last for seconds to minutes
- warning signs of cerebrovascular disease and impending stroke
- Motor speech and language deficits most common symptoms of TIAs
44
Q
Aneurysms
A
- balloon-like malformations in weakened areas of arterial walls
- most commonly found in internal carotid, anterior or middle cerebral arteries
45
Q
Intracerebral Hemorrhage
Infarcts
A
- Cerebral hemorrhage - vessel ruptures into brain, accumulation of blood in neural tissue (intraparenchymal or intracerebral hemorrhage)
- often associated with :
- elevated blood pressure
- chronic hypertension
- Symtoms appear abruptly and are focal but can progress cause of mass effects from blood accumulation.
- Common sites of intracerebral hemorrhage:
- thalamus
- basal ganglia
- brainstem
- cerebellum
46
Q
Subarachnoid
Hemorrhage
(SAH)
A
- most common extracerebral hemorrhage
- vessel ruptures on the surface of brain and blood spreads over its surface and throughout the subarachnoid space.
- Onset - abrupt
- Symptoms & pathologic changes - diffuse
- common cause - ruptured aneurysms, rupture of (AVM) arteriovenous malformation (collection of abnormally formed veins and arteries)
47
Q
4 Major Divisions of
Speech Motor
System
A
- Final Common Pathway
- Direct Activation Pathway
- Indirect Activation Pathway
- Control Circuits
48
Q
Final
Common
Pathway
(FCP)
A
-
Basic Function- Stimulates muscle contraction and movment
- other motor divisions must act through it to influence movement
-
Major Structures -
- Cranial Nerves
- Spinal Nerves
- Related Designations - Lower motor neuron system
- referred to as LMN system (Lower motor neuron system)
- peripheral mechanism through which all motor activity is mediated
- Last link in the chain of neural events that lead to movement.
49
Q
Effects of Damage
to FCP
A
- damage to one nerve = weakness or paresis if all alpha motor neurons in muscle are not damaged
- no input from all LMNs = paralysis
- muscles lose bulk and atrophy
- abnormal spontaneous motor unit activity & lower firing threshold
- = fasciculations ( brief localized twitches)
- = fibrillation -slow repetitive action potentions & contract regularly
- Damage responsible for speech characteristics of Flaccid Dysarthria
50
Q
Final Common Pathway
& Speech
A
- FCP for speech includes:
- paired cranial nerves that supply muscles involved in phonation, resonance, articulation & prosody
- paried spinal nerves involved in speech breathing and prosody
- V- Trigeminal Nerve
- VII - Facial Nerve
- IX - Glossopharyngeal Nerve
- X - Vagus Nerve
- XI- Accessory Nerve
- XII - Hypoglossal Nerve
51
Q
Trigeminal
Nerve
V
A
- largest of cranial nerves
- sensory functions -
- transmission of pain
- thermal & tactile sensation from face and forehead
- mucous membranes of nose and mouth
- teeth
- portions of cranial dura
- conveys deep pressure and kinesthetic information from teeth, gums, hard palate and temporomandibular joint & jaw
- innervates:
- muscles of mastication & mylohyoid
- anterior belly of digastric
- tensor tympani
- tensor veli palatini muscles
-
Effects of damage:
- LMN lesions of masticatory nucleus/axons = paresis/paralysis and eventual atrophy of masticatory muscles on paralyzed side
- Unilateral trigeminal nerve lesions = no major effects on speech
- Bilateral lesions = devastating; jaw hangs open, cannot be closed, moves with limited range–>preventing facial, bilabial & lingual articulatory movements from achieving accurate place & manner of articulation.
52
Q
Facial Nerve
VII
A
- paired; mixed motor and sensory nerve
- motor component - supplies muscles of facial expression & stapedius muscle (only clear role in speech)
- sensory component - innervate submandibular, sublingual, lacrimal glands, taste receptors on anterior 2/3 of tongue, & nasopharynx
-
Effect of Damage-
-
LMN lesions - weaken or paralyze muscles of entire ipsilateral side of face
- affects all voluntary, emotional, & reflex movements
- atrophy = facial asymmetry; fasciculations in perioral area & chin
-
LMN lesions - weaken or paralyze muscles of entire ipsilateral side of face
53
Q
Vagus Nerve
X
A
- paired; complex & lengthy
- mixed motor & sensory nerve
- important functions for speech
- Motor functions include innervation of :
- striated muscles of soft palate
- pharynx
- larynx
- Sensory role:
- transmission of sensation from same motor structures
- Additional functions:
- parasympathetic innervation to & sensation from thorax and abdominal viscera
- sensory innervation from external auditory meatus & taste receptors in posterior pharynx
-
3 branches relevant to speech - at exit from skull through jugular foramen
- pharyngeal branch - responsible for pharyngeal constriction & retraction and elevation of soft palate during velopharyngeal closure for speech and swallowing.
-
superior laryngeal nerve branch -
- internal - sensory; carries sensation from mucous membrane linicng larynx down to level of vocal folds, epiglottis, base of tongue, aryepiglottic folds & dorsum of arytenoid cartilages; transmits info from muscle spindles and stretch receptors to larynx
- external- supplies inferior pharyngeal constricor & cricothyroid muscles; especially important for phonation; cause cricothyroid lengthens voal folds for pitch adjustments.
-
recurrent laryngeal branch - doubles back on itself before reaching larynx
- responsible for laryngeal sensory & motor activiites involved in phonation & swallowing
-
Effects of damage - effects depend on branch of nerve where damage is
- all branches - weakness of soft palate, pharynx, larynx
- Unilateral LMN lesions - affects resonance, voice quality, and swallowing but usually affect phonation more prominantly than resonance
-
Bilateral LMN lesions - devastating effects on resonance & phonation
- secondary significant effects on prosody and precision of articulation
- swallowing may be significantly impaired
54
Q
Accessory Nerve
XI
A
- also called spinal accessory nerve
- has cranial and spinal portion
- cranial - contributes fibers to uvula, levator veli palatini & intrinsci laryngeal muscles, while intermingled with vagus nerve fibers
- spinal - innervates sternocleidomastoid & trapezius muscles
-
Effects of damage -
- Foramen magnum area lesions (where ascending nerve enters skull) or Jugular foramen (where it exits skull) = weakens head rotation toward side opposite of leasion (sternocleidomastoid weakness)
- also reduces ability to elevate or shrug shoulder on side of lesion
- Foramen magnum area lesions (where ascending nerve enters skull) or Jugular foramen (where it exits skull) = weakens head rotation toward side opposite of leasion (sternocleidomastoid weakness)
55
Q
Hypoglossal Nerve
XII
A
- paired motor nerve
- innervates all intrinsic and all but one of the extrinsic muscles of tongue (exception is palatoglossus, supplied by vagus nerve).
-
Function: receives taste and tactile information from nucleus of tractus solitarius & sensory trigeminal nucleus
- important for speech, chewing, swallowing & sucking
-
Effects of damage:
- atrophy, weakness, & fasciculations of tongue on side of lesion
- unilateral weakness = tongue deviates to side of lesion when protuded.
56
Q
Direct Activation
Pathway
A
- has direct connection & influence on FCP
- also known as pyramidal tract or direct motor system
- Divisions:
- corticobulbar - influences activities of cranial nerves
- corticospinal tract - influences activity of spinal nerves
- together = Upper Motor Neuron (UMN) system
- has major influence on cranial and spinal nerves that form the FCP for speech production.
- directly connects the cortex to the FCP
- facilitative effect on FCP
- leads to movement (not inhibition of movement), presumably finely controlled, dexterous, and discrete movements, such as those required for speech.
- Origin- Cerebral cortex
- Destination- Cranial and spinal nerve nuclei
- Function- Direct voluntary, skilled movements
-
Distinctive signs of lesions -
- weakness and loss of skilled movement/dexterity
- hyporeflexia
- decreased muscle tone
- Babinski sign
57
Q
Upper Motor
Neuron (UMN)
System
A
- controlled directly or indirectly by the cortex, cerebellum, and basal ganglia
- refers only to the direct & indirect activation pathways
- part of motor system that is contained entirely within CNS
- does not include the basal ganglia or cerebellum
- does include the direct and indirect activation pathways & control circuits
58
Q
Direct Activation
Pathway
Functions
& Effects of Damage
A
-
Function - crucial to voluntary motor activity
- consciously controlled skilled, discrete & rapid voluntary movements
- movements are triggered by specific sensory stimuli not not considered reflexes because they are voluntary and not stereotyped
- movements are generated by cognitive activity & involves complex planning which speech falls into.
-
Effects of Damage -
- lesions produce weakness and loss or reduction of skilled movements (not as profound as that associated with LMN lesions).
- UMN lesion unilateral - weakness is on opposite side of body because FCP & peripheral sensation are not part of direct activation pathways.
- minor effects on jaw movement & velopharyngeal, laryngeal, and breathing for speech
- frequently cause some tongue weakness on the side opposite the lesion.
- contralateral lower facial weakness can be quite prominent after unilateral UMN lesions.
- can produce dysarthria that seems to reflect weakness with loss of skilled movement (unilateral UMN dysarthria).
- Bilateral UMN lesions -
- mild to devastating effects on speech
- reflects effects of direct and indirect activation pathways dysfunction
- spastic dysarthria- reflects bilateral weakness with loss of skilled movement & alterations in muscle tone (spasticity) as result of indirect activation pathway involvement
59
Q
Indirect Activation
Pathway
A
- Origin- Cerebral Cortex
-
Destination- Cranial and spinal nerve nuclei
- influences activities both gamma and alpha motor neurons in FCP
- Gamma motor neurons more sensitive –> responds more reaily to indirect motor system.
-
Function - Control posture, tone and movements suportive of voluntary movement
- regulates reflexes maintaining posture, tone, & activites that provide framework on which direct activation pathway can accomplish skilled, discrete actions
- subconscious & require integration of activities of many supporting muscles
- ensures speciic speech movements occur without constant or variable interference with their speed, range, and direction.
-
Distinctive Signs of Lesions-
- Spasticity (and weakness)
- Clonus
- Hyperactive stretch reflexes
- increased muscle tone
- Decorticate or decerebrate
- aka extrapyramidal tract, indirect motor system, brainstem motor pathways (regions where multiple synapses occure before reaching FCP are located mostly in brainstem)
-
Effects of Damage -
- Lesions- affect muscle tone & reflexes; primarily manifest as spasticity & hyperreflexia
- Corticoreticular fiber lesions above midbrain & nucleus - tends to extend legs and resist bending; arms flex and resist extension (decorticate posturing)
- Midbrain below red nucleus but above vestibular nuclei - remove arm flexor excitation and result in excitation of all extensor muscles and generalized increase in extensor tone (decerebrate posturing)
- Below medulla lesions - loss of all descending input and produce generalized flaccidity in muscles supplied by spinal nerves
- brainstem lesions that damage reticular formation - often lead to death
- Dysarthrias: spastic dysarthria when lesions are bilateral & unilateral UMN dysarthria when lesions are unilateral.
60
Q
Cerebellar Control Circuit & Speech-
Structures
A
- Two components:
- flocculonodular lobe - has primary connections to vestibular mechanism for modulating equilibrium & orientation of head & eyes
- primary function - control of eye movement
- body of cerebellum includes:
- midportion (vermis)
- lateral cerebellar hemispheres
- both can be subdivided into anterior and posterior lobes
- anterior - projection area for spinocerebellar proprioceptive information; important for regulating posture, gait, and truncal tone
- posterior lobe- hemispheres important for coordinating skilled, sequential voluntary muscle activity.
- Somatotopic organization invuding of speech structures (lips & tongue) is evident in portions of both lobes
- each hemisphere is connected to contralateral thalamus & cerebral hemisphere - each helps control movements on ipsilateral side of body.
- flocculonodular lobe - has primary connections to vestibular mechanism for modulating equilibrium & orientation of head & eyes
-
Purkinje cells - output neurons of cerebellar cortex;
- purkinje cell axons synapse deep cerebellar nuclei, structures form whih cerebellar output departs through the peduncles
- nuclei includes: dentate, globose, emboliform and fastigial nuclei
- Dentate - important for speech; active in initiating movement, executing preplanned motor tasks, and regulating posture
- damage: associated with persisting dysarthria
- Dentate - important for speech; active in initiating movement, executing preplanned motor tasks, and regulating posture
61
Q
Cerebellar
Control Circuit -
Function
A
-
Function -
- general role in speech; recieving advanced notice about syllabic content of utterance from cortex so it can refine properties of physical expression.
- helps coordinate timing among components of movement
- scale the magnitude of muscle action
- coordinate the sequence of agonist and antagonistic muscle activity
- all necessary for speech production
- plays role in adjusting stored patterns of syllables and syllable production patterns for execution of prosodically normal utterances with appropriate rate and tempo, linguistic & emotional stress, etc.
- specific contributions to speech is uncertain, but definitely present due to imaging and presence of speech disturbances from cerebellar damage.
62
Q
Cerebellar Control
Circuit -
Effects of Damage
A
- Flocculonodular lesions - truncal ataxia (inability to stand or sit without swaying or falling), gait disturbances, nystagmus (repetitive, jerky eye movements), & other ocular movement abnormalities
- Lesions of caudal vermis - gait ataxia
- Lesions in lateral and paravermal cerebellar hemisperes - associated with intention tremor & incoordination of voluntary movements
- incoordination reflected in dysmetria (impaired estimation of range of motion)
- dyssynergy or decomposition of movement (parts of movement are produced in segmented sequences instead of smoothly)
- dysdiodokinesia (abnormal timing & velocity of alternate movements)
- lesions affect limb movements (limb ataxia) and can lead to dysarthria.
- effects on speech of cerebellar lesions = inccordination & hypotonia (ataxic dysarthria)
- Bilateral Vermis/cerebellar hemisphere damage or cerebellar output pathways in brainstem = more serious consequences for speech than damage elsewhere in circuit.
63
Q
Basal Ganglia
Control Circuit
Structures
A
- paired; have cognitive, affective & motor control functions
- Input- Putamen receives excitatiory input fro prefrontal cortex, as does STN (subthalamic nucleus); also receives input from SN (substantia nigra); nigrostiatal pathway crucial to control of movement
-
Intracircuit inhibition & excitation -
- 3 intrinsic pathways -
- cortex to putamen to internal segment of globus pallidus (GPi)–>leads to inhibition of GPi
- cortex to putamen to external segment of Global Pallidus (GPe) to STN –>increases GPi activity
- cortex to the STN–>increases activity in GPi
- Putamen inhibits GPi, STN excites globus pallidus
- 3 intrinsic pathways -
- Output- output pathways originate in GPi. Inhibitory fibers go to thalamus for relay back to SMA & prefrontal motor areas of frontal lobe –>important for movement initiation; influence muscle tone and movement;
-
Neurotransmitter balance:
- motor functions driven by several neurotransmitters
- dopamine - influences sensitivity of neurons to excitatory & inhibitory input
- ACh - opposes or offsets effects of dopamine
- glutamate- excitatory function for STN to GPi input
- GABA - released from efferent fibers from striatum to GPi & GPi - SN
- imbalance can degrade control of motor performance, lead to movement disorders (incl. dysarthrias) associated with several basal ganglia diseases
- motor functions driven by several neurotransmitters
64
Q
Basal Ganglia
Control Circuit
Functions
A
- opening gates to intended movements, closing gates to competing or unwanted movements, preventing “locking up” of movement
- facilitates or inhibits specific movemnts
- relative to speech:
- posture & tone regulation: regulating muscle tone & maintaining normal posture; contributes to control of movements that accompany and facilitate goal directed activities (chewing, walking, speaking with restricted jaw movement)
- movement scaling: scaling the force, amplitude, duration, speed of movements during the execution of motor plans
- set switching: interrupting ongoing behavior to prepare and facilitate appropriate nonroutine responses to noel stimuli or changing circumstances
- movement selection & learning: helps build repertoire of movements that can be triggered in response to appropriate stimuli
65
Q
Basal Ganglia
Control Circuit-
Effects of Damage
A
Can be manifested in two general ways:
- reduced mobility = hypokinesia (too little movement)
- Involuntary movements = hyperkinesia (too much movement)
66
Q
Hypokinesia
A
- often associated with disease of SN (Substantia Nigra)
- results in deficiency of dopamine in basal ganglia
- = increase in muscle tone, unlike in spasticity, is not velocity dependent & is present throughout the range of motion of limbs
- =increased resistance to movement (rigidity: slow & stiff movements and may be initiated or stopped with difficulty)
- restriction of movement is shown in reduced range of movement underlying many of deviant speech characteristics of hypokinetic dysarthria.
- also can be caused by drugs that block dopamine receptors (antipsychotics & antiemetics) & certain toxins.
- face can become “masked” or expressionless.
67
Q
Hyperkinesia
A
results from excessive activity in dopaminergic nerve fibers–> reducing circuit’s damping effect on cortical release of unwanted, competing motor programs.
- = involuntary movements (e.g. chorea, athetosis, dystonia) that can vary in locus, speed, regularity, & predictability.
- movements underlie many deviant speech characteristics associated with hyperkinetic dysarthria
