n165 quiz 4

language

a bidirectional system of expression of thoughts as signals thru oral and written and interpretation of those signals as thoughts thru comprehension. infinite possible combinations where hearing and auditory processing becomes language/code that becomes the final concept/message. speech production is opp with concept/message, language/code, motor planning/sequencing, and then articulation/exectution.

language and the brain

basic auditory perception spectrotemporal analysis to phonological network that travels along the ventral stream for language comprehension in the combinational network and lexical interface of the temporal lobes that together becomes the conceptual network with the dorsal stream for speech production in the articulatory network and sensorimotor interface. of the parietal and frontal lobes. the left hemisphere has a functional specialization for language

aphasia language

loss of ability to understand or express speech caused by brain damage. not a result of deficits in sensory intellectual or psychiatric functioning or muscle weakness. classified by specific deficits present. not specific to ear mouth channel the damage is to a general language function as apparent in signers where they have difficulty using their hands and fingers for communication despite retaining movement.

aphasia treatments

production aphasias do better with rehab than with comprehension aphasias. various speech therapy paradigms like speech entertainment are being tested. compensation mechanisms have also developed in other regions of cortex.

brocas aphasia/ expressive aphasia

speech output is difficult and lacking functional words. problems with grammar, articulation, and rely on high frequency content words. severe deficits in repetition, severe in naming, normal comprehension, and severe in fluency.

wernicke’s aphasia/ receptive aphasia

fluent but meaningless speech, semantic errors and little understanding of what language is. associated with anosognosia a deficit of self awareness and typically evolves into less severe conductive aphasia or anomic aphasia. moderate to severe deficits in repetition, severe to mild in naming, severe in comprehension, and paraphasic fluency where one loses the ability of speaking correctly by inappropriately changing words.

transcortical aphasias

transcortical sensory similar to wernicke’s aphasia except able to repeat with no comprehension. cant comprehend what is said but can speak fluently. transcortical motor similar to broca’s aphasia except able to repeat but with mild comprehension problems, associated with right hemiparesis. cant produce spontaneous speech but in mild cases can form hesitant speech.

paraphasia

literal/phonological paraphasia more than half of the spoken word is said correctly. neologistic paraphasia less than half of the spoken word is said correctly and occasionally not at all. verbal paraphasia substitutes another word for the target word.

conduction aphasia

classical model suggests damage to arcuate fasciculus the white matter tract connecting temporal and frontal cortex. hickok model suggests damage to area Spt. deficits are poor repetition, poor naming, normal comprehension, and normal fluency.

global aphasia

severe communication difficulties may be completely non verbal linked to difficulties with speech and comprehension. caused by extensive damage to left cortex around lateral fissure associated with right hemiparesis.

transcortical mixed aphasia

same as global aphasia but able to repeat. the Broca's area, Wernicke's area, and the arcuate fasciculus are intact but the watershed region around them is damaged isolating these areas from the rest of the brain.

anomic aphasia

recalling words or names is severely impaired where patients resorts to circumlocution usually from damage to parietal and temporal lobes. specific forms of words may be lost like in averbia the loss of verbs and color anomia the loss of color names.

auditory verbal agnosia/ pure word deafness

the inability to perceive spoken speech with a mostly intact auditory perception for complex non speech sounds, the ability to have intact speech themselves, and can read and write normally. often exhibit deficits in perceiving other rapid sounds like amusia caused by bilateral damage to temporal lobes.

dysarthria communication

motor disorder affecting any or all of the four subsystems of speech respiration, phonation, resonance, and articulation. symptoms and classification dependent on type of nervous system involvement

spastic dysarthria

upper motor neuron damage located in the cortex restricting inhibitory motor info to a specific spinal cord level caused by cerebral palsy, strokes, or multiple sclerosis. symptoms are harsh strained voices, vocal pitch breaks, and reduced speed of articulation.

flaccid dysarthria

lower motor neuron restricting constriction damage caused by brainstem strokes, cranial nerve palsy, and myasthenia gravis the most common form of MG. symptoms are reduced lip closure from reduced strength of articulatory muscles and hypernasality causing a breathy voice.

other types of dysarthria

hypokinetic like parkinsons where prominent symptoms are muscle rigidity and inability of movement. hyperkinetic like huntingtons where prominent symptoms are unwanted or excess movements. ataxic like cerebellar damage is a neuro sign consisting of lack of voluntary coordination of muscle movements. mixed applies to subtypes of many disorders with a combo of symptoms.

apraxia communication

speech disorder linked to problems with speech production not muscle weakness. symptoms are difficulty putting sounds and syllables together in the correct order to form words with ppl often groping for the right word. can either be developmental seen as a disorder to a child’s ocerall language development or a neuro disorder that affects the brains ability to send proper speech muscle signals or acquired occurring with muscle weakness affecting speech dysarthria or damage to the nervous system aphasia.

language gene

KE family observed developmental verbal apraxia but also other language deficits across half the family for 3 generations possibly caused by mutation of FOXP2.

stuttering

a speech disorder where flow of speech is disrupted by involuntary repetitions and prolongations of sounds syllables words phrases and involuntary silent pauses. unknown causes but therapy includes relaxation techniques singing and choral reading.

cluttering

a fluency disorder with problems with rate, word confusion, disorganized thoughts most clear at the start of speech but rate increases and intelligence decreases towards the end. causes unknown and ppl often unaware of disorder so therapy focuses on speech details.

cluttering examples

spoonerisms phonemic substitution. malapropisms wrong word substitutions. freudian slips error in speech from unconscious mind.

sinus organization

inhale draws airs thru the nasal sinuses, directing it up the cavity using the inferior middle and superior turbinates where it can be picked up by the olfactory epithelium lining only the top of the cavity. the cribriform plate separates the frontal lobe from the nasal cavity and within its many holes are olfactory receptor neurons that have axons leading to the frontal lobe olfactory bulb.

olfactory receptor cells

100 million bipolar nerve cells derived from the CNS located in the olfactory epithelium where the mucosal end forms a knob that has 4-25 olfactory hairs that project into the mucus. this cilia forms a dense mat that reacts to odors in the air to stimulate the olfactory cells.

olfaction requirements

substance must be volatile, slightly water soluble to pass thru the mucus of the olfactory cilia, and slightly lipid soluble to pass thru the lipid membrane of the cilia.

trigeminal nerve

the fifth cranial nerve that serves as a sensory nerve of face teeth mouth and scalp but also carries motor nerves for chewing muscles. measures touch pressure pain and temps in eye mouth and nasal cavity as 70% of odors produce different sensations.

olfactory epithelium to bulb

little is known about how taste and smell is encoded after odors are picked up the the olfactory receptor neurons but likely organized into some kind of topographic map. the axons pass thru the cribriform plate to form axons of olfactory nerve filaments called glomerulus that synapse onto mitral cells that help form the olfactory tract in the bulb. the receptor neruons undergo continuous neurogenesis. axons leading to the olfactory bulb is CNS but the olfactory epithelium is PNS.

olfactory bulbs

2 multi layered structures located on the ventral surface of the brain that receives feedback from cortex that can modulate olfactory perception. may play a role in identification of odor type and concentration

cortex olfactory processing

only sensory pathway that does not first pass thru the thalamus otw to the cortex. more ancient pathway using spatial temporal olfactory bulb and tract inputs that projects onto the olfactory tubercle and piriform cortex that act as the primary olfactory cortex where odor id and concentration take place. from here next stage in reward system at the orbitofrontal secondary ofractory cortex that evaluates whether you like the smell or not using context and prior experience. connection to limbic systems emotion and memory of higher order olfactory processing in the amygdala and entorhinal cortex within unclear steps.

anosmia and hyposmia

the complete loss of smell could be congenital or acquired from trauma, dementia, nasal spray damage, smoking, etc. similar to anosmia hyposmia is the decreased sensitivity to odors

phantosmia

hallucinated smell often unpleasant likely resulting from overactivity of the olfactory cortex seen in epilepsy.

dysosmia and hyperosmia

with dysosmia things smell differently than they should often unpleasant while with hyperosmia theres an abnormally acute sense of smell both seen in pregnancy

olfaction and gustation

chewing brings the smell of the food up the nose as regular smell while also releasing molecules from the breakdown of food as odorants that lift up to the receptors using the turbinates as retro-nasal smell.

tongue structure

most numerous filiform papillae purely break apart and move the food, vallate papillae are large and in the back with taste buds in the groove, foliate papillae located on the sides, and fungiform papillae with tastebuds on the surface located in front. all taste buds have an outer taste pore with microvilli that protrude from the top end of each taste receptor cell and interact with tastant molecules. the taste receptor cells connect to the gustatory nerves and how they interact depends on the kind of receptor.

tongue peripheral taste organ

tastant molecules must be small to medium size, able to dissolve in saliva, then enter the taste pore where it can bind to receptors, change the receptor potential, and form an action potential

supertasters

have more fungiform papillae that are more tightly arranged so each taste bud has more papilla and thus more gustatory nerve endings. results in increased sensitivity to bitter taste and the texture of fat.

gustatory pathways

taste buds and gustatory neurons in tongue and throat feed to brainstem then thalamus where it projects to the primary somatosensory cortex S1 for texture and the primary gustatory cortex anterior insula/frontal operculum for taste id and intensity. primary feeds to the secondary orbitofrontal cortex and feeds heavily on the reward pathway and signals satiety.

taste disorders

aguesia the loss of taste, hypoguesia the decreased sensitivity to taste, and dysgeusia abnormal taste. caused by medication, vitamin deficiencies, respiratory illnesses, and nerve damage.

tongue disorders

geographic tongue inflammatory condition leads to loss of papillae caused possibly by burns infections or medication. fissured tongue may be painful or painless associated with geographic tongues associated with aging environmental factors and genetic conditions.

grapheme color synesthesia

word form and visual color processing near each other. individual letters and numbers evoke specific colors with no common agreement of letter color combos across ppl.

lexical gustatory synesthesia

spoken or written words evoke vivid sensations of taste but can also be triggered by corresponding food names or words that share phonemes.