damage to right parietal lobe or anterior superior temporal cortex (name and disorder)
phonagnosia - difficulty recognizing voices
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speech meaningful, mot fluent send motor commands to mouth area of pmc (premotor cortex)
( I, Cup, me -not i want cup)
brocas aphasia
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fluent speech, but canât understand, production meaningless, patient unaware (saying too many words that don't make sense, nonsense speaking)
Wernickeâs aphasia
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Canât understand speech, canât repeat or write heard words, but can spontaneously speak, read, write, understand nonâspeech sounds, read lip - type of wernicke aphasia
auditory verbal agnosia AVA
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damage to posterior language area - can repeat speech but canât understand it (name and area of brain)
Transcortical sensory aphasia - brocas
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damage to arcuate fasciculus - can understand speech but canât repeat (name and area of brain)
Conduction aphasia -brocas
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alexia and agraphia
inability to read and inability to write
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speech and language functions are lateralized in the brain with circuits for comprehension and producted located in the ( ) hemisphere
left
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which hemisphere play a role in processing emotional content, rhythm, and stress of speech and language
right
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3 areas involved in perceptions of current events and memories
occipital, parietal, temporal
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area that control muscle of speech, involve with speech and language perception
brocas area
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changes in intonation, rhythm, and stress that add meaning to language
prosody
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what type of aphasia affect prosdy
brocas aphasia
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Identify the brain regions involved in recognizing peopleâs voices.
part of brain that connects wernicke and brocas area
arcuate faculus
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blood vessel obstruction
cerebrovascular accident
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diificulty comprehending, repeating, or producing meaningful language
aphasia
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severing the corpus collosum and treat seizures
split brain operation
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left temporal lobe produce disorder of auditory word recognition
pure word deafness
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speaking in a roundabout way, individuals who have anomia
circumlations
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Ěś sensation that precedes seizure, exact nature depends on location of seizure focus
aura
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often seen in children, characterized by periods of inattention which are not subsequently remembered
absence (petit mal) seizure
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generalized, tonicâclonic seizure, which results in convulsion
grand mal seizure
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Ěśseizure where patientâs skeletal muscles are contracted
tonic phase
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seizure where patient shows rhythmic jerking movements
clonic phase
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condition in which patient undergoes series of seizures without regaining consciousness
status s epilepticus
caused by excessive release of glutamate during seizure
status epilepticus
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seizures treatment
anticonvulsant drugs, surgery
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CVA caused by rupture of cerebral blood vessel
hemorrhagic stroke
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CVA caused by occlusion of blood vessel
ischemic stroke
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interruption of blood supply to region of body
ischemia
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blood clot that forms within blood vessel
thrombus
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piece of material that floats from one part of vascular system to block another part
embolus
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surgery, anticoagulant drugs, tissue plasminogen activator (tPA) breaks down blood clots, Desmoteplase (anticoagulant glycoprotein found in the saliva of vampire bats)
cardiovascular accident treatment
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neurodegeneration due to repeated head trauma, prevalent in athletes, confirmed by postmortem examination
Chronic Traumatic Encephalopathy
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reduce swelling and intracranial pressure, assure adequate blood flow, treat symptoms that develop after injury, assess long term behavioral and cognitive changes
treatment of brain injury
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â˘accumulation of abnormally folding prion proteins in brain which triggers apoptosis (programmed cell death)
Transmissible Spongiform Encephalopathies
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causes intellectual disability, usually tellâtale physical abnormalities
⢠Fetal Alcohol Syndrome
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inherited absence of enzyme that converts phenylalanine to tyrosine. Accumulation of phenylalanine causes brain damage unless special diet implemented soon after birth
⢠phenylketonuria (PKU
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extra 21st chromosome, moderateâtoâsevere intellectual disability, physical abnormalities, brain degeneration in adulthood (similar to Alzheimerâs)
Downs Syndrome
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â inherited metabolic disorder in which certain gangliosides (type of lipid) accumulate in neurons and destroy them. Symptoms appear around 6 months old, death occurs usually by age 4. More common with Jewish heritage. No cure or treatment.
TayâSachs Disease
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⢠brain looks spongy ⢠contagious, affects humans and other animals ⢠examples: CreutzfeldtâJakob Disease (human form of Bovine Spongiform Encephalopathy), Fatal Familial Insomnia
Transmissible Spongiform Encephalopathies
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degeneration of nigrostriatal DA neurons projecting to striatum (caudate and putamen) of basal ganglia
Parkinsonâs disease
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may be partly caused by a misfolded protein called Îąâsynuclein (probably needed for DA release) which accumulates in, and kills, DA neurons
Parkinsonâs disease
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resting tremor ⢠muscle rigidity ⢠difficulty initiating movement ⢠slow movement and shuffling gait
receptors also involved in reinforcing effects of opiates, alcohol, cocaine, nicotine
cb1
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⢠resting tremor ⢠muscle rigidity ⢠difficulty initiating movement ⢠slow movement and shuffling gait ⢠postural instability ⢠some cognitive deficits
Parkinson disease
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parkinson has at least two mutations have been identified which affect blank accumulation
Îąâsynuclein accumulation
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works initially â crosses BBB, but as more DA neurons die, more drug causes sideâeffects, including psychosis (parkinson treatment)
levodopa
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parkinson drug that reducing symptoms but not slowing disease
deprenyl
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⢠hereditary, caused by dominant gene on chromosome 4 ⢠mutation produces an abnormal version of a protein now known as huntingtin (Htt) which misfolds, accumulates, and causes apoptosis
huntington disease (no treatment)
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hunting disease causes degeneration of (blank) (caudate nucleus and putamen) which disinhibits premotor and supplementary motor areas, causing motor symptom
striatum
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⢠degeneration of blank and blank ⢠symptoms: spasticity (increased tension of muscles, causing stiff and awkward movements),
spinal cord and cranial nerve motor neurons
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ALS treatment: , (blank) a drug that reduces glutamateâinduced excitotoxicity, probably by decreasing the release of glutamate, patients live two months longer
riluzole
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⢠Autoimmune demyelinating disease â immune system attacks the myelin ⢠affects transmission of neural messages at various locations in CNS, causing a variety of symptoms that diffER BETWEEN PATIENTS
Multiple Sclerosis (MS)
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process leaves hard patches of debris called sclerotic plaques
multiple sclerosis
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in Lewy body dementia, Lewy bodies are found in the cortex and other brain areas and also affect BLANK transmission
ACH
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alzheimer is usually old age, more blank than blank
women than men
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cause of alzheimer
degeneration of brain areas that receive ACh projections
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â˘alzheimer diseas has blank â dense core of ď˘âamyloid protein (which accumulates in AD brains) surrounded by dying axons and dendrites and activated microglia and astrocytes
amyloid plaques
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â dying neurons containing accumulations of (blank) filaments that formerly made up cellâs internal skeleton
tauâprotein
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anterograde amnesia due to thiamine deficiency usually caused by chronic alcoholism
Korsakoffâs Syndrome / Dementia
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AchE inhibitors help symptoms until disease is advanced ⢠NMDA receptor antagonist slow excitotoxic death of Ach neurons ⢠amyloid vaccine seems promising, but brain inflammation in 5% of patients halted study, so new immune techniques in the works
alzheimer treatment
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inflammation of brain caused by bacteria, viruses, or toxic chemicals
inflammation of brain caused by bacteria, viruses, or toxic chemicals
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viruses that can cause encephalitis:
herpes, rabies, polio
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â inflammation of meninges caused by bacteria or viruses
Meningitis (rash)
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psychotic symptoms which can be treated with antipsychotics
⢠disordered thought and speech â shifts from one subject to another with vague connections (word salad) ⢠delusions â false beliefs that persist despite contradictory evidence ⢠grandeur, persecution
Schizophrenia (positive affects)
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: absence of normal behaviors ⢠flat affect, avolition, social withdrawal ⢠poor hygiene and grooming ⢠poverty of speech and movement ⢠distorted sense of time
schizophernia negative affect
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higher incidence in children of older fathers, probably mutations in spermocytes
schizpphrenia genetic link
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reduced volume in what part of brain cortex (large ventricles), correlated with negative symptoms
hippocampus, amygdala, thalamus, prefrontal
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in schizophrenia, loss of blank may disrupt coordination of brain areas, correlated with both positive and negative symptoms
white matter connections
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traditional antipsychotics block blank receptors in schiophrenia
d2
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partial agonist - reduce positive and negative symptoms ⢠drug with very high affinity for a particular receptor type, but activates receptor less than normal ligand does ⢠serves as agonist in regions of low concentration of normal ligand and as antagonist in regio
, aripiprazole (Abilify)
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serves as agonist in regions of low concentration of normal ligand and as antagonist in regions of high concentrations in what disease
schizophrenia (dopamoine hypothesis)
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⢠too blank in some areas may directly or indirectly (via DA and/or 5âHT systems) cause both positive and negative symptoms (schizophrenia)
little glutamate
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⢠abuse of PCP (glu antagonist) â positive and negative symptoms ⢠1: PCP â indirectly increase DA activity in Nac ⢠2: PCP â indirectly decrease DA utilization in PFC
positive and negative
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Major Depressive Disorder (drugs)
(MAO inhibitors, tricyclics, SSRIs) affect NE and/or 5âHT
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â˘suicidal people have lower levels of
CSF 5âHIAA
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Major Depressive Disorder: Treatments
tricyclic antidepressant, that block 5âHT and NE reuptake
short pulses of electric current passed through right hemisphere (sometimes bilateral for suicidal patients), causing seizure, requires anesthesia and hospital stay ⢠works fast, but shortâterm, so not used chronically (mostly for suicidal or treatmentâ resistant patients)
ECT , electroconvulsive therapy
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⢠depression, lethargy, sleep disturbances, and craving for carbohydrates during the winter season when days are short
Seasonal Affective Disorder (SAD)
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BIPOLAR DISORDER TREATMENT 3
lithium, ⢠Depakote, Tegretol
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ptsd brain changes in blank (more reactive) and blank (reduced volume)
amygdala, hippocampus
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GAD brain
perhaps insufficient BZD receptors, perhaps oversensitive ANS, overactive amygdala that is not being quelled by PFC
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anxiolytics shortâterm, antidepressants longâterm ⢠benzodiazepines (mild tranquilizers) (Valium, Librium, Xanax) ⢠may cause drowsiness, must avoid alcohol, can become tolerant, relapse after discontinuing medication ⢠TCAs, SSRIs, SNRIs used longâterm, especially SSRIs â˘DCS (NMDA indirect agonist) with CBT
GAD and panic disorder treatment
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ocd treatment
⢠SSRIs (clomipramine, fluoxetine, fluvoxamine) (requires higher dose, not due to antidepressant effects) block obsessions ⢠DCS (NMDA agonist) combined with CBT
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a chronic spectrum disorder involving differing levels of compulsive, ritualistic behavior, impaired sociability, mental retardation
autism
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adhd medication
methylphenidate (Ritalin) inhibits DA and NE reuptake
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LTP in VTA strengthens excitatory synapses on DA neurons, increases activation of NAC and dorsal striatum (and other structures) causing learned behaviors associated with substance abuse
synaptic plasticity, learning
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opium and substance p
inhibit the release of substance p which causes pain
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methadone
similar to heroin, but in pill form, so slow acting and long lasting ⢠relieves craving and blocks euphoria ⢠cheap, saf
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opioid antagonist that blocks opioid receptors ⢠used to treat opiate overdose and addiction