Neuro Notes Week 10.1 PDF

Exam 3 Week 10 Neuro notes Cognitive Communication Disorders -Difficulties with communication competence (listening, speaking, reading, writing, conversational interaction) that result from underlying cognitive impairments (attention, memory, organization, information processing, problem-solving &...

Exam 3 Week 10 Neuro notes Cognitive Communication Disorders -Difficulties with communication competence (listening, speaking, reading, writing, conversational interaction) that result from underlying cognitive impairments (attention, memory, organization, information processing, problem-solving & executive functions). -Cognitive function is a broad term that refers to mental processes involved in the acquisition of knowledge, manipulation of information, and reasoning. Cognitive functions include the domains of perception, memory, learning, attention, decision-making, and language abilities.  Acquired Brain Injuries  Impairment of brain function  Acquired after birth (not genetic)  Not during the birth process  Non-Progressive Acquired Brain Injuries:  Stroke (CVA) Aneurysm, hemorrhage  Loss of oxygen (hypoxic brain injury, anoxia)  Brain tumors  Infection: encephalitis, meningitis, Lyme disease, West Nile  Intervention effects: chemotherapy, surgical complications  Seizure disorders  Electrocution  Traumatic Brain Injury (TBI)  CVAs (Stroke)  Hemorrhagic  Hematoma  Ischemic  TIAs  May Result in: Aphasias  *May also result in: Cognitive Communication Disorder Loss of Oxygen  *Hypoxic Brain Injury: Partial supply of oxygen available, but inadequate to maintain normal brain function  *Anoxic brain injury: Complete obstruction of oxygen supply to brain Brain Tumors  *Tumor: Mass of abnormal cells that form in your body  *Tumor=neoplasm  Different types of tumors including:  *Medulloblastoma: tumor starting in the medulla–pediatric  *Glioma: tumor originating in brain or spinal cord from glial cells. *Glioblastoma is the most malignant form of glioma and is the most common type of malignant brain tumor in the United States  *Meningioma: a tumor that grows in the meninges  Infections  *Encephalitis  Brain swelling due to inflammation (from autoimmune, cancer, drugs/toxins)   *Meningitis  Inflammation of the meninges of brain/spinal cord. Caused by virus, bacteria, parasites  Lyme Disease  Bacterial infection from infected insect, tick. Starts with a ring-shaped rash. (infection may spread to brain)  West Nile virus  Mosquito born disease, RNA virus (infection may spread to brain)  Intervention Effects  *Chemotherapy  Uses drugs to kill cancer cells or preventing multiplication of them  Treats cancer by shrinking the tumor  Reduces risk of cancer return  Slows/stops growth  ‘chemo brain’: Cognitive impairment is an adverse reaction of cancer chemotherapy and is likely to affect up to 75% of patients during the treatment and 35% of patients experience it for several months after the chemotherapy  *Seizure disorders  *Epilepsy: neurological disorder involving having two or more unprovoked seizures that occur more than 24 hours apart  Chronic brain conditions that cause repeated seizures  Seizure occurs when there is a burst of abnormal electrical activity in the brain and may lead to temporary brain dysfunction  Symptoms:  Loss of consciousness  Muscle contractions  Jerking or twitching  Changes in emotions of behavior  Seizure disorders  Many different kinds/typed of seizures, including:  *Absence Seizures (petit mal): Person ‘staring into space’ temporarily  *Tonic seizures: Cause stiffening of muscles (usually arms, legs, back)  *Clonic seizures: Repeated jerking on both sides of the body  Seizure disorders  Causes: often unknown Result of genetics or brain injury, brain tumors  Sometimes, high fever: febrile seizure (does not meet criteria for epilepsy, usually only happens once)  Cognitive impairment People with epilepsy are at increased risk for cognitive impairment  Electrocution  Result of electric shock that causes severe injury to the body (machinery, lightning, appliances, taser)  Effects depend on how long body is exposed and frequency of current  Burns, heart issues → hypoxia, CNS damage Vessels may hemorrhage  TBI: Traumatic Brain Injury TBI: Background Information  * Coup: injury occurs under the site of impact with an object  * Contrecoup: injury occurs on side opposite area that was hit  Acceleration-deceleration injury: in motor vehicle accidents  Damage in frontal +temporal lobes  Both coup and contrecoup will coincide with one another.  *Diffuse axonal injury: Brain tissue are compressed, torn apart + sheared on bony prominences of skull Etiology Cognitive Communication Difficulties Motor Vehicle Confrontation naming, verbal reasoning, speed of reading, conversational Falls discourse, verbal fluency, comprehension and procedural discourse. Blunt Trauma Blast Injury Word retrieval, disorganized expression, dysfluency, conversation in noise & groups, planning, problem solving, decision making, learning. Sports Concussioon Word retrieval, complex comprehension, executive functions, academic performance. Penetrating Brain Discourse- Narrative length, Story grammar, Completeness Site of lesion Injury not significant Length of *post-traumatic amnesia(PTA): loss of memory TBI: Severity of Traumatic Brain Injury * Measured using: 1. Glasgow Coma Scale (GCS) lower scores → worse 2. Duration of Coma prolonged period unconsciousness longer time → worse 3. Post-traumatic Amnesia (PTA) longer time → worse TBI: Severity of Traumatic Brain Injury * Measured using: 1. Ranchos Los Amigos is another scale…  * TBI: SLP + Traumatic Brain Injury  In addition to possible other deficits depending on location + severity of injury:  Training to self monitor use of compensatory strategies  Vocational + social training  Pragmatics  10.2 Notes:  Neural Networks  Memory  Neurocognitive disorders *A cognitive network is a system of connected brain regions that work together to perform specific mental tasks, l 1. Default Mode Network: The DMN is primarily active when a person is at rest or engaged in internal thought processes rather than focused on the external environment includes brain regions like the medial prefrontal cortex, posterior cingulate cortex, and parts of the parietal lobes *Function: social aspects of language or memory-dependent speech tasks 2. Salience Network: Responsible for switching between the DMN and the Central Executive Network based on contextual relevance Interior insula and anterior cingulate cortex *Function: enables individuals to detect changes in the environment or in conversation, helping them adapt their responses. Damage to this network could lead to challenges with attention and emotional regulation, affecting interpersonal communication and the ability to stay focused 3. Central Executive Network: *Supports high-level cognitive processes like working memory, problem-solving, and focused attention Dorsolateral prefrontal cortex and parietal regions *Function: goal-directed tasks or complex thought processes, such as organizing speech or following multi-step instructions _____________________________________________________________________________________________________ Neurocognitive Processes: Memory Short Term Memory (STM): temporarily holds and processes new information Prefrontal cortex and parietal lobes Limited capacity, seconds to minutes unless rehearsed essential for tasks like reading or holding onto information briefly before it’s either forgotten or transferred to long-term memory Phone number, someone’s name, someone’s address  *Working Memory (STM)  extension of STM but is more complex, involving active manipulation of information  Dorsolateral prefrontal cortex, parietal lobe  allows for real-time processing & data integration  Critical for language comprehension, reasoning, problem-solving  Remembering someone’s address—while actively planning/mapping a route to it, Building on new information learned in class   Long Term Memory (LTM)  type of memory has a virtually unlimited storage capacity  Hippocampus, temporal and parietal lobes, basal ganglia, cerebellum (skills and habits), amygdala (emotional)  Long Term Memory (LTM) Divided into: Explicit (Declarative) Memory: Includes facts and events. ▪ Episodic Memory: Memory for personal experiences and specific events, such as recalling past conversations (where were you during 9/11?) ▪ Semantic Memory: General knowledge about the world, such as vocabulary and facts independent of personal experiences. (grass is green, DC is capitol of USA) Implicit (Non-declarative) Memory: Often unconscious and includes skills and learned behaviors, like motor skills required for speech articulation, riding a bike, navigating your home  reticular Activating System (RAS)  network of neurons in the brainstem that regulates sleep-wake cycles, arousal, and consciousness Damage to the RAS can result in reduced attention span and issues with maintaining focus, critical for patients with traumatic brain injuries or neurodegenerative conditions  Altered mental status(AMS)  mental function that stems from illnesses, disorders and injuries affecting your brain  leads to changes in awareness, movement and behaviors. Symptoms: Confusion Reduced alertness Odd behavior Hallucinations Changes in consciousness. Changes in movement Changes in cognitive function Due to: Infections Chemical imbalances Chronic diseases like diabetes or COPD Head injuries Certain medicines Alcohol or drugs Neurodegenerative Diseases: Dementia: Umbrella term for a range of neurological conditions that lead to progressive cognitive decline - Affecting cognitive processes:memory, thinking, problem solving and of often behavior  Dementia: Alzheimer’s Disease Lewy Body Vascular Frontotemporal Mixed Dementia  *General Symptoms of Dementia Memory Loss: Short-term memory is often affected first, with challenges recalling recent events or new information. Language Problems: Difficulty finding words, following conversations, or understanding speech. Disorientation: Trouble recognizing familiar people, places, or situations. Behavioral Changes: Increased irritability, apathy, or inappropriate social behavior. Problem-Solving Difficulties: Struggles with complex tasks or decision-making. Alzheimer’s Disease  Alzheimer’s Disease  most common form of dementia  affecting memory, language, and cognitive functions  primarily impacts episodic memory—the ability to recall specific events or experiences—and progresses to impair other types of memory and reasoning skills.  Brain Areas Affected:  AD starts in the hippocampus and entorhinal cortex, regions crucial for memory formation, before spreading to the temporal and parietal lobes. As it advances, it affects the frontal lobes, impairing executive functions like planning and decision-making. rogression: progresses through mild, moderate, and severe stages: Mild AD: Early symptoms include forgetfulness, difficulty finding words, and slight issues with spatial orientation. Moderate AD: Worsened memory, confusion, and difficulty with complex tasks arise, alongside noticeable personality changes. Severe AD: Individuals lose the ability to communicate, recognize loved ones, and require full-time care as brain function is broadly impaired. Pathology: AD is characterized by beta-amyloid plaques and tau tangles in the brain, which damage and kill neurons, disrupting neural communication and memory. Frontotemporal Primarily affecting personality, behavior, and Dementia (FTD) language before memory. It manifests in two main types: Behavioral Variant (bvFTD): Causes changes in personality, empathy, and social conduct. Primary Progressive Aphasia (PPA): Affects language skills, leading to difficulties in speaking, understanding, and reading. Brain Areas Affected: frontal and temporal lobes. Progression: Symptoms progress differently from Alzheimer’s & Parkinson’s:  Early Stages: Behavioral changes, apathy, and language difficulties are more prominent than memory loss. Mid to Late Stages: As it advances, FTD can impact memory and movement, making it harder to distinguish from AD or PD. Pathology: FTD may involve abnormal proteins such as tau or TDP-43 in the affected brain regions, leading to neuron loss and cortical atrophy in the frontal and temporal lobes. Lewy Body Dementia *Pathology: buildup of abnormal protein deposits (LBD): called Lewy bodies within brain nerve cells. *Symptoms: Besides cognitive decline, LBD can cause vivid hallucinations, attention fluctuations, and difficulties with movement, making it distinct from other types of dementia. Also, motor symptoms similar to Parkinson’s. Parkinson’s Disease Affects motor function but also leads to cognitive & (PD) memory impairments. Brain Areas Affected: PD is caused by the degeneration of dopamine-producing neurons in the substantia nigra→movement. Cognitive symptoms arise as disease progresses→prefrontal cortex & hippocampus. Progression: PD starts with motor dysfunction, cognitive later Early Stages: Tremors, rigidity, and bradykinesia (slowness of movement) are primary symptoms, with minor cognitive effects. Mid to Late Stages: Cognitive decline appears, including memory issues, slow thought processes, and dementia in some cases. Language and executive functions like planning can also be affected. *Pathology: PD’s pathology includes the presence of Lewy bodies (abnormal protein deposits) in neurons, contributing to cell death in brain areas crucial for motor control and cognitive functions.  Huntington’s Disease  Autosomal dominant *genetic disorder caused by a mutation in the HTT gene, leading to progressive brain cell degeneration.  *HD affects motor function, cognition, and behavior, making it both a movement disorder and a cognitive disease. Speech and language are progressively impaired. *Brain Areas Affected: HD initially affects the basal ganglia (particularly the caudate nucleus and putamen), which disrupts motor control and executive functions. As the disease progresses, it impacts the cerebral cortex, leading to cognitive and emotional symptoms. Multiple Sclerosis *Autoimmune disease where the immune system attacks the myelin sheath (protective covering) of nerve fibers, leading to communication issues between the brain and body. Brain Areas Affected: MS lesions can appear in various brain and spinal cord areas, affecting the white matter that connects different regions. These lesions impact cognitive processes, memory, and language, depending on their location __________________________________________________________________________________________ Development of the Nervous System Embryology CNS PNS Neuronal Migration Primitive Reflexes  Development of the Nervous System *3 primary germ layers: *Ectoderm Skin, hair, nails…and… Nervous system! Mesoderm: Muscle and connective tissue Bones and cartilage Blood Vessels Endoderm Digestive tract Lungs, liver, pancreas Embryonic Period: Week 3 Notchcord: cellular rod forms direct thickening of ectoderm to form neural plate On day 18 neural plate begins to fold an fuses, going on to form the neural tube, completed by the end of week 4. Neural Tube: a narrow channel that forms in an embryo during the third and fourth weeks of pregnancy and develops into the brain and spinal cord *Somites: As neural tube rises from ectoderm, cube-like structures form from columns from the mesodermal layer. Somites differentiate into: muscles, bone, and connective tissue (nonneural) Early Development: Pharyngeal Arches(4th week) *Four brachial/pharyngeal arches develop in head area 1→ Bones, jaw, and muscles of mastication 2, 3, 4→ muscles and cartilages of face, larynx, and pharynx 4th week continued: - PNS rises from neural crest - Also arises from specialized epidermal cells called placodes. - Placodes and neural crest cells form ganglia of CN V, VII, VIII, IX, and X Early development: Cranial and caudal ends of neural tube become more differentiated From neuroectoderm: neuroprogenitor cells flourish *Neuroprogenitor cells migrate and differentiate to form specific areas of the brain Within weeks 3-4 Process: Neurulation: Weeks 3-4 *Primary neurulation Process of formation of brain and spinal cord through to lumbar vertebrae *Secondary neurulation Process by which caudal neural tube gives rise to sacral and coccygeal vertebrae Neural Tube → Mature CNS - Anencephaly: Defect in primary neurulation. Failure of anterior tube closure. Can cause facial deformities, unformed brain with possible absent skull. - 100% lethal within first year of life Spinal Dysraphism: Posterior neural tube fails to completely close: cleft of lower spinal column. -Closed: skin covering cleft -open: obvious cleft Spinal cord formation: *The basal plate (front) forms the motor neurons, and the alar plate (back) forms the sensory neurons. *Meninges come from early embryonic cells. *Ventricles develop from the neural tube, which also forms the brain. Early brain development: These vesicles split into key parts: hindbrain, midbrain, and forebrain. *The forebrain divides further to form regions like the thalamus, basal ganglia, and cortex. *Midbrain = midbrain *Hindbrain becomes the medulla, pons, and cerebellum. The brain's surface starts folding at 20 weeks, forming gyri and sulci, which increase its surface area  Cortical Layering: The cortex (outer brain layer) develops in an “inside-out” manner, with earlier neurons staying close to the origin and later neurons migrating past them to form layers. Migration Mechanisms: Somal Translocation: Early neurons use this method, moving from their starting point to the brain’s outer layer. Glia-Guided Locomotion: As the brain develops, neurons use radial glial cells as a guide, moving along them to their final locations. Synapse Formation: After reaching their location, neurons develop axons and dendrites to connect with other neurons. Axons grow and connect through growth cones at their tips, which guide them toward target cells. Some connections are strengthened through use, while others may disappear if not needed *Critical Periods and Teratogens: The brain is most vulnerable to harmful factors (teratogens) from weeks 3 to 16 of pregnancy. Environmental factors, like drugs or toxins, can impact brain formation and lead to intellectual disabilities. Diagnosis of Neurological Disorder with Primitive Reflex Primitive reflex profile * Important to understand the development of motor reflexes Diagnosis of Neurological Disorder with Primitive Reflex Primitive reflex profile Orderly appearance + disappearance * Beginning in fetal period + extending through 1st year * If not on schedule: at risk for cerebral injury or other neurologic impairment * Peak development ~ 6 months * Testing at peak development allows for: early diagnosis of disturbed motor function early intervention _______________Primitive Reflexes____________________________________________ -Asymmetric Tonic Neck Reflex (ATNR) - Most Widely Known early body reflexes When a healthy child is supine (face + torso facing up) may lie with head turned to one side  extremities on that side are extended contralateral extremities are in corresponding flexion “fencer’s position” * If response found past 8th or 9th month, indicative of: possible cerebral damage and poor motor development * Symmetric Tonic Neck Reflex * analogous to ATNR When a healthy child is prone Head is manipulated in flexion + extension (not turned laterally) causes arms to flex + legs to extend * If response absent at 5-6 mos. or persists into 2nd year, indicative of: Motor abnormality * Positive Support Reflex Infant is suspended around trunk, below armpits With head in midline + slightly flexed Bounced on balls of feet X 5 Feet then place in contact with floor: Test degree to which infant attempts to support their weight Flexion at hips + knees If not integrated beyond 4 months, associated with: spastic quadriparesis Segmental Rolling Reflex development of motor reflexes Eventually, turn into more permanent movement patterns  * Galant Reflex Arching of infant’s body when skin of back near vertical column is stroked Should laterally flex toward stimulated side Normally disappears by 2 months of age but Persists in athetosis…- slow involuntary twisting of upper limb + speech muscles w varying degree of hypertonia in between movements. Moro Reflex * Along with ATNR: one of best-known reflexes Testing: With sudden head lowering rapid + symmetric abduction + upward movement of arms hands open then, gradual adduction + flexion of arms lower limbs also show extension then, flexion Peaks at 2 months → diminishes by 4 months Persistent reflex associated with: Cerebral Palsy Intellectual disability * Tonic labyrinthine reflex (TLR) Tested in both supine + prone positions Links vestibular sense to proprioceptive to help develop a sense of balance * Abnormal TLR: - common in children with pathologic conditions - routinely associated with oral reflexes - when head extended 45˚: a reflex tongue thrust may occur in child with CP _____________________Oral_pharyngeal Reflexes______________________ Studies show weak correlation between reflex abnormalities and the severity of dysarthria Dysphagia symptoms are slightly better predictors of articulation issues. *Feeding: Managed by brainstem reflex pathways. *Feeding therapy may help muscle control but does not directly impact speech skills. Rooting Reflex Testing: touch cheek next to mouth Reflex: head turn toward stimulus  grasp stimulus in mouth Integration: disappears 3 – 6 months age replaced by direct head-turning response direct head-turning response disappears by end of 6th month * Suckling Reflex Testing: finger or a nipple placed in infant’s mouth Reflex: Rhythmic bursts of suckling behavior interspersed with periods of rest Integration: Involuntary suckling disappears 6 – 12 mos. Age * Swallowing Reflex Testing: saliva accumulation or bolus of food in pharynx Reflex involves muscles of: Coordinated movement of mouth, tongue, palate, + pharynx Integration: continues throughout life immature swallow w tongue thrusting sometimes seen until ~18 mos. * Tongue Reflex Testing: touch lip or tongue Reflex: Tongue thrusts between lips Part of suckle-swallow reaction Cranial Nerve: XII Integration: * Bite Reflex Testing: moderate pressure on gums Reflex: jaw closure and a bite response CN V Integration: Disappears 9 – 12 mos. age Replaced with more normal chewing pattern  Gag Reflex Testing: touch posterior half of infant tongue or touch posterior wall of pharynx Reflex: Rapid velopharyngeal closure Protective measure for esophagus CN IX, X Integration: Present at birth Continues throughout life Testing Cranial nerves in children: -CN V: Trigeminal - Testing: when confronted w small bolus on lips or tongue child should initiate voluntary mastication  Aim is to determine whether: - Bolus can be pulverized - Food can be m,anipulated to back of oral cavity  Abnormal: abnormal mastication, may limit child to only eating diced or liquefied food  CN VII: Facial  Testing: small food bolus on lower lip in midline observe oral reaction  Aim is to determine whether:  Purposeful use of muscle of lips + lower face  Disorders:  Lack of smiling response  Asymmetricl smile: possible unilateral paresis  Lack lip tonicioty: inadeqwuate lip seal - Drooling may result  CN XII: Hypoglossal  CN XII: Hypoglossal - Testing: retrieve food from lower lip licking - Aim is to determine whether child/infanct can shape point, protrude tongue Pediatric speech disorders - Cerebral Palsy - Neurological condition - Cause: injury to immature brain  Etiology: prematurity, anoxia, birth trauma, infection  *CP is a neurological condition resulting in a movement disorder *CP types based on: localization brain damage severity of damage * All Cerebral Palsy (CP): Damage to: 1 of 3 areas of brain involved in movement 4 CP types (* + Mixed CP: e.g., spastic-ataxic: stiff + shaky) spectrum of movement impairment  * Cerebral Palsy is a Neurological Condition Characterized by non-progressive disturbance of motor system *Types: 1. Spastic > stiff , tight muscles > level of cortex + pyramidal tract 2. Dyskinesia > uncontrolled movements, +/- athetosis > basal ganglia + extra pyramidal tract 3. Ataxic > shaky, clumsy, unstable/incoordination> cerebellum 4. Mixed … i.e. spastic + ataxic , stiff and shaky Classified by muscles involved: hemiplegia, paraplegia, diplegia, quadriplegia *Plegia: loss of voluntary movement Hemiplegia: ½ one side body Paraplegia: lower ½ body Diplegia: symmetrical parts (can be both symmetrical arms + legs) Quadriplegia: all 4 limbs 1. Spastic cerebral palsy: most common CP: * Localization: damage to: Motor cortex +/or UMN of pyramidal tracts recall: pyramidal because thru medullary pyramids to spinal cord Spastic cerebral palsy * Movement impairment: Stiff muscles of arms or legs Movements difficult, laborious, jerky, unusually slow Walking may be stiff Falls from not reacting quickly enough to regain balance Hypertonic (too much muscle tone) reflexes: Very brisk response (too strong or too many times) or clonus Pediatric Speech Disorders: Cerebral Palsy 1. *Spastic CP + SLP: Spastic hemiplegia: ½ one side body Developmental delay in phonology + language Possible Cognitive disturbances Spastic paraplegia: lower ½ body  Speech WNL Usually no significant cognitive impairment Spastic diplegia: symmetrical parts (both arms or both legs) Usually, all 4 with > lower extremity difficulties: “scissors gait” Possible dysphagia + drooling Spastic Dysarthria: Mild – Severe With more severe dysarthria, also show: Respiratory, laryngeal, palatal, +pharyngeal impairment Not all have cognitive impairment 1. *Spastic CP + SLP: Spastic quadriplegia: all 4 limbs Both corticospinal + corticonuclear tracts involved This type has highest incidence of intellectual disability or developmental delay * Major difficulties: Respiration, spastic dysarthria, laryngeal movement Hypernasality Compromised palatal + pharyngeal musculature 2. Athetoid (dyskinetic) Cerebral Palsy 5 – 10 % of all CPs * Localization: Basal ganglia +/or Extrapyramidal tracks: Recall: to other brain structures ( not through medullary pyramids) 2. Athetoid (dyskinetic) Cerebral Palsy * Movement impairment: Dyskinetic quadriplegia: usually all four limbs involved Hypotonia: abnormally low level of muscle tone Note: Can fluctuate between Stiff + Flaccid (floppy) Involuntary movements Twisting, clenching, abrupt, random Worsens when stressed  gone when sleeping Hard to maintain posture / stay upright Sitting balance is delayed or not developed 3. Ataxic CP: * Movement impairment: Hypotonic muscles Unsteady, shaky movements  Under- + over- shooting to grab Shaky standing/walking leads to falls Incoordination of upper + lower extremities Disturbed balance Wide gait to achieve more stability + balance May not be able to steady on feet: staggering, lurching May not be able to steady arms on walker Can be shaky in muscles of face + throat Making it difficult to speak or swallow Muscular Dystrophy *Caused by a genetic mutation e.g., Duchenne MD is associated with sex- linked recessive gene recall: to have a trait that is expressed by a recessive gene More common in males given only 1 X sex chromosome *Muscular Dystrophy Early development milestones are often delayed Often language milestones are delayed as well Language delay associated with later cognitive impairment Intellectual disability in 1/3 cases Characteristic progression of muscle weakness starting in pelvis + trunk Eventually involving all striated muscles, including those of speech Following CP, Muscular Dystrophy is most common reason for childhood dysarthria Muscular Dystrophy + SLP * Articulation disorder (can be mild) Articulator weakness: Tongue: Rate of movement + strength are poor In advanced cases: broadening + flattening of tongue Lip retraction + pursing is impaired Muscular Dystrophy + SLP * Flaccid dysarthria: Voice quality disturbance Respiratory + laryngeal muscles are weakened Respiratory weakness + phonatory performance Reduced oral breath pressure  Reduced vocal intensity *Spinal Muscular Atrophy (SMA) SMA is a genetic disorder that affects the motor nerve cells in the spinal cord, leading to muscle weakness and atrophy. Unlike MD, SMA specifically impacts the nerves that control muscle movement rather than the muscles directly. Progressive muscle weakening and wasting *Childhood Apraxia of Speech Neurological speech disorder that affects a child's ability to plan and sequence the movements needed to speak Awkward movement of speech muscles not attributed to developmental dysarthria No structural lesion or evidence of dysfunction found * Childhood Apraxia of Speech Speech symptoms Difficulty in motor planning + execution: poor accuracy of movement Slow diadochokinetic rate Inconsistent errors in repeated productions of syllables + words Poor accuracy of vowel productions Sound substitutions not necessarily related to target sound Often vocal or nonvocal groping behaviors Inappropriate prosody at word + phrase level * Childhood Apraxia of Speech CAS assessment Assessments with most sensitivity: maximal performance for multisyllabic word production + prosody DEMSS Dynamic Evaluation of Motor Speech Skill Early intervention is key Pediatric Disorders of Language (aka Language delay) -By far most prevalent language impairments In childhood are developmental (not acquired) At birth brain weight: 25% of adult brain weight, adult is 3 lbs 1 year old: 60% of adult weight 5 years brain is 90% of full growth 12 years: brain reached full brain weight Most cortical neurons are in place at birth Another way brain growth may be measured is through development of synaptic connections + myelination... * Myelination development 1st: Precentral gyrus develops myelination first 2nd: Somatosensory area myelination Primary Visual Cortex completed soon after birth * Primary Auditory Cortex continues beyond first year * Cortical association areas lag behind primary cortex areas * Inferior parietal lobe not fully myelinated until adulthood, well into fourth decade * Arcuate fasciculus connecting Broca’s + Wernicke’s areas -begins myelination in 1st year + continues afterward Language lateralization o Genetically predetermined pattern of asymmetry o Further reinforced under specific environmental influences o In righthander: 95% left brain dominated for language o In left-Hander: 50% to 70% left brain dominated for language Language dominance * Left hemisphere shows early structural differences That supports later language dominance Sylvian fissure is longer in the left hemisphere Planum temporale is larger in the left hemisphere (triangular region of the brain that plays a key role in language processing and auditory functions) * Broca’s area is not differentiated until 18 months * Corpus callosum is not myelinated until 10 years… Callosal Dysgenesis: absence of part or complete rostral corpus callosum Children show developmental delay because poor communication between left and right brain hemisphere Cerebral plasticity: brain more plastic during rapid periods of brain growth The younger the child, the more quickly language disturbance resolves if left hemisphere damage before end of year 1 make it less likely for language to have functional reorganization ( language shifting to right brain. Acquired childhood aphasia Developed language normally then sustain a trauma to brain The earlier lesion onset, the better the prognosis * Uninjured hemisphere completely takes over language function due to plasticity Cerebral plasticity Each area of cortex has a critical period * so child’s recovery depends on: -where lesion occurred + critical period for that part of brain -Environmental stimuli has significant effects during critical period Parental interactions w children are key in developmental of language, social skills, personality development Behaviors associated w abuse or neglect often lead to developmental milestone delays, including speech + language delays Signs of abuse may include: Extreme behavior outbursts Self-destructive behaviors Poor academic performance Language delays * Environmental factors: Lack of social support Poverty Homelessness or poor-quality housing *Bilingual code switching is not a deficit Language disorder: impairment in comprehension +/or production of language form, content, or use * Language difference: variation in a symbol system that reflects and is determined by shared regional, social, or cultural-ethnic factors