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What results from damage to the descending lateral motor system in the spinal cord?
- inability to form voluntary, goal-oriented movements with distal limbs (contralateral)
- does not affect postural control
Damage to which part of the brainstem generally results in ataxia?
What are the general functions of the midbrain?
eye movt; pupillary light reflex (CN3); orienting, ”consciousness”
What are the general functions of the pons?
sensory info from face (CN5); control of facial (CN7) and chewing (CN5) mm, lateral eye movt (CN6); corneal blink reflex (CN5,7)
What are the general functions of the medulla?
gag reflex (CN 9,10); swallowing, tongue movt (CN 12); regulation of CVS, respiratory and visceral activity
What is the cause of multiple sclerosis and what are its symptoms?
- cause: demyelination of CNS; axonal loss
- sx: optic neuritis, weakness, spasticity, ataxia, tremor, cognitive damage
What are the patterns of sensory loss with damage to the brain, brainstem, and spinal cord?
- brain: hemisensory; unilateral
- brainstem: hemisensory; crossed face-body; unilateral
- spinal cord: sensory loss at level of lesion; bilateral; head okay
Which diseases primarily affect UMN only?
primary lateral sclerosis
Which diseases primarily affect LMN only?
- spinal muscular atrophy
- viral infections (e.g. polio, HIV, etc.)
Which diseases primarily affect UMN and LMN concurrently?
amyotrophic lateral sclerosis (ALS)
What are some examples of association bundles in the brain?
- intrahemispheric bundles
- superior longitudinal fasciculus (frontal, temporal, parietal, occipital lobes) (includes arcuate fasciculus)
What are some examples of projection fibers?
What are the components and locations of the primary sensory cortex?
- somatosensory cortex: postcentral gyrus
- visual cortex: banks of calcarine fissure
- auditory cortex: transverse temporal gyri
- olfactory cortex: perpyriform cortex at junction of orbitofrontal and temporal lobes
What are the components and locations of the primary motor cortex?
primary motor cortex = precentral gyrus
Where is the premotor cortex?
- posterior part of superior and middle frontal gyri (e.g. frontal eye fields)
- sometimes included as part of the association cortex
Which area of the brain has the highest level of dopamine innervation?
What are some general features of the prefrontal cortex?
- highest amount of dopamine innervation in brain
- heteromodal, higher order association cortex
- connected with amygdala (directly and via MD nucleus)
What are some general functions of the prefrontal cortex?
- restraint: inhibition of inappropriate behavior
- initiative: motivation to pursue productive activity
- order: capacity to perform meaningful sequences of motor activity
- working memory
- mental flexibility
- selective attention
What generally results from lesions to the prefrontal cortex?
- impaired executive function
- inappropriate jocularity
- environmental dependency
- problems with abstract reasoning and judgment
What results from a lesion to the orbito-frontal part of the prefrontal cortex?
- abulic state
What results from a lesion to the dorso-lateral part of the prefrontal cortex?
- disinhibited behavior
- poor judgment
How does damage to the left prefrontal cortex differ from damage to right prefrontal cortex?
- damage to the left prefrontal cortex --> depression
- damage to right prefrontal cortex --> mania
How do schizophrenia and prefrontal cortex relate?
damage to prefrontal cortex or abnormalities in dopaminergic circuits may relate to schizophrenia
What are some general features of the temporal lobe?
- contains continuation from primary visual cortex of the "what" stream (i.e. object identification)
- bidirectionally linked with hippocampus
What are some general functions of the temporal lobe?
- contains continuation from primary visual cortex of the "what" stream (i.e. object identification)
- relearning of visual form discriminations
- consolidation of memories
- some olfactory function
What generally results from damage to the temporal lobe?
- visual agnosias
- (bilateral) Kluver-Bucy syndrome
- memory problems
What generally results from electrical stimulation to the temporal lobe?
- sensations of deja vue, religious or mystical phenomena
- strange dream-like experience
- olfactory hallucinations
What are some general functions of the parietal lobe?
- spatial analysis (especially non-dominant hemisphere)
- contains continuation from primary visual cortex of the "where" stream (i.e. localization of object)
What genreally results from lesions to the parietal cortex?
- anosognosia (lack of awareness of illness or condition)
- hemi-attention in one or more sensory modalities
- abnormal internal representation of spatial details
- astereognosis (inability to identify an object by touch without visual input)
What is the function of the occipital association cortex?
higher order visual areas
dorsally: "where" stream concerned with location/movement of visual objects; spatial relationships (projects to parietal lobe)
ventrally: "what" stream concerned with identification of objects (projects to temporal lobe)
What generally results from legions to the occipital lobe?
- visual agnosias: prosopagnosia (damage to fusiform gyri bilaterally)
- achromatopsia (inability to perceive color)
seizures in occipito-temporal cortex can produce complex visual hallucinations
What are some general (lateralized) functions of the left cerebral hemisphere?
- handedness, eyeness, speech
- language (verbal)
- concepts (ideas)
- analytic (logical)
- sequential (details)
- arithmetic (linear)
- immediate verbal memory (word recall)
What are some general (lateralized) functions of the non-dominant (right) cerebral hemisphere?
- visuo-spatial tasks, emotional significance of stimuli, spatial attention, music
- musical (nonverbal)
- pictures (pattern recognition)
- synthetic (artistic)
- holistic (big picture)
- geometric (spatial)
- immediate nonverbal memory (visual or melodic recall)
Apraxia (loss of language function, loss of detailed analytic ability, loss of complex motor programming) results from damage to which cerebral hemisphere?
- dominant cerebral hemisphere
- (generally left hemisphere in most people)
Which cortical layers receive input from other cortex?
layers II, III
Which cortical layers send outputs to other cortex?
layers II, III, V, VI
Which cortical layers receive afferents from thalamus?
layers III, IV
Which cortical layers send outputs to thalamus?
In which cortical layer do projection fibers (corticostriatal, corticopontine, corticobulbar, corticospinal, corticothalamic) originate?
- layer V: corticostriatal, corticopontine, corticobulbar, corticospinal
- layer VI: corticothalamic
What is the definition of epilepsy?
abnormal, excessive, paroxysmal (sudden and transient), synchronous discharge of a population of neurons, with a change in behavior and/or perception
What are the 4 main types of general seizures?
- tonic-clonic (grand mal)
- absence (petit mal)
- myoclonic: twitches, jerks
- atonic: sudden loss of muscle strength
What part of the brain is the most common origination point for focal seizures?
What are the 4 stages of an "epileptic's life"?
- aura: brief period at start of some seizures; patient remembers brief period; can give clues to seizure origination site (e.g. weird smell)
- ictus: sequence of events that form seizure itself
- post-ictal: immediately after seizure; symptoms during this period will vary depending on type/severity of seizure
- inter-ictal: all the rest of epileptics life
What is the general progression of a focal seizure?
- originates in one part of cortex (esp. temporal)
- partial (focal) seizure (aura)
- cortex interacts with deep brain nuclei
- seizure spreads (generalization)
- post-ictal period
What is the fundamental cause of an interictal epileptiform discharge?
- paroxysmal depolarizing shift
What is cerebral palsy and what are its clinical features?
- cerebral palsy = static encephalopathy = syndrome of delayed and abnormal motor development due to dysfunction of the CNS
- clinical features:
- static encephalopathy that does not progress
- spastic weakness
- sometimes involuntary movements
- may also have epilepsy, cognitive impairment
What are some potential causes of cerebral palsy?
- insults to developing nervous system
- neonatal or perinatal hypoxia
- *most have no identifiable cause*
What are some clinical features of intellecutal disability (mental retardation)?
- sub-average intellectual abilities (IQ less than 70)
- limitations in adaptive functioning
- non-progressive syndrome (vs. cognitive degenerative disorders that may lead to dementia)
What are the (4) classic clinical features of hypotonia in children/infants? What are some additional "clues" for differential diagnosis?
- paucity of voluntary movements
- unusual postures
- decreased resistance to passive movement of a joint
- increased joint mobility
abnormal deep tendon reflexes (UMN vs. LMN/Peripheral/NMJ)
What are the 2 basic clinical patterns of hypotonia in children?
- paralytic: floppy, weak --> peripheral nervous system disease
- non-paralytic: flppy, adequate muscle strength --> central nervous system disease
Which is false about the thalamus?
a. the thalamus projects primarily to the cerebral cortex
b. all sensory pathways, except olfactory, synapse in the thalamus
c. many thalamo-cortical projections are reciprocal
d. there are no points of contact between the thalami in either hemisphere
- d. there are no points of contact between the thalami in either hemisphere
- (interthalamic adhesion)
What structure lies between the posterior lobes of the thalami?
What are the sensory nuclei of the thalamus?
- ventral posterior medial (VPM): somatosensory from face
- ventral posterior lateral (VPL): somatosensory from body
- lateral geniculate nucleus (LGN): visual
- medial geniculate nucleus (MGN): auditory
What are the motor nuclei of the thalamus?
- ventral anterior (VA): basal ganglia, cerebellum
- ventral lateral (VL): cerebellum, basal ganglia
What are the association nuclei of the thalamus?
- lateral dorsal (LD)
- lateral posterior (LP)
- pulvinar (P)
What are the (7) major types of nuclei in the thalamus?
- intralaminar (e.g. centromedian)
What are the limbic nuclei of the thalamus?
- anterior (A): mammillary bodies
- medial dorsal (MD): hypothalamus
What separates the thalamus into anterior, medial, and lateral portions?
internal medullary lamina
Through which structure do thalamic outputs project to the cortex?
What are the general inputs and outputs of the motor thalamic nuclei (VL, VA)?
- inputs: globus pallidus (VA); cerebellum (VL)
- outputs: premotor,supplementary motor areas (VA); motor, premotor areas (VL)
What behavior is the intralaminar nuclei of the thalamus involved in?
Which thalamic nuclei projects to the cingulate gyrus?
Which thalamic nuclei projects to the prefrontal cortex?
Which thalamic nuclei project to the superior and middle frontal gyri?
Which thalamic nuclei project to the parietal, occipital, and temporal lobes?
Which thalamic nuclei project to the parietal lobe?
Which thalamic nuclei project to the postcentral gyrus?
What are some thalamic projections through the internal capsule and where are they located?
- thalamic radiations (i.e. thalamo-cortical fibers): both limbs
- anterior limb: anterior/medial thalamic nuclei --> frontal lobe
- posterior limb: ventral thalamic nuclei --> motor and sensory gyri
Where is the retrolenticular radiation of the thalamus and what does it connect?
- retrolenticular radiation is behind the lentiform nucleus (i.e. posterior margin of posterior limb of internal capsule)
- connect: LGN --> visual cortex
Where is the sublenticular radiation of the thalamus and what does it connect?
- sublenticular radiation is below the lentiform nucleus
- connects: MGN --> auditory cortex
What is autism?
- autism is a continuum of disabilities:
- impaired social development
- impaired communicative development
- restricted or repetitive behaviors
assessment is qualitative: relative to developmental level or mental age
What are some examples of autism spectrum disorders?
- Asperger's syndrome
- pervasive developmental disorder otherwise not specified (PDD-NOS)
What are some clinical presentations of autism spectrum disorders?
- deficits in social communication/interaction (lack of social reciprocity, failure to develop/maintain social relationships)
- restricted, repetitive patterns of behaviors, interests, activities
- impaired higher level processing
- mood instability
- imitation impairments
- slowed face learning
- decreased amygdala activity
- enlarged brain
What are some factors that contribute to positive outcomes of childhood-diagnosed autism?
- degree of MR
- language ability
- neurophysical impairment
- other symptom profiles
What behavior pattern are mirror neurons associated with?
- imitation behavior
- (inferior frontal gyrus, inferior parietal lobe, superior temporal sulcus, premotor cortex)
What are some potential causes for the associated enlarged brain in autistic children?
- increased neuronal proliferation
- decreased programmed cell death
- decreased axonal elimination
- decreased dendritic pruning
What are the stages of sleep and some basic characteristics?
- stage 1: EEG activity low
- stage 2 : EEG activity high
- stage 3/4: EEG activity high
- stage REM: fast, desynchronized rhythms in cortical EEG, autonomic activation, loss of muscle tone, REM
- NREM stages = 80% of sleeping cycle
- full sleep cycle: 4-6 in a night; 90-110 minute intervals
How does REM sleep compare to NREM sleep?
- first episode = longest in sleep cycle
- first episode = shortest in sleep cycle
What nervous system components are involved in circadian rhythms?
- suprachiasmatic nucleus (SCN, hypothalamus): "central pacemaker" (light cycle)
- DMH (dorsal medial nucleus of hypothalamus)
- supraparaventricular zone (SPZ)
- medial preoptic area (MPO)
- ventrolateral preoptic area (VLPO)
- paraventricular nucleus
- lateral hypothalamic area (LHA)
- arcuate nucleus
- pineal gland: melatonin production (dark cycle)
- adenosine (accumulates during wake to threshold--> promotes sleep)
What are some key components of the ascending arousal system?
- Ach input to thalamus (dorsal route)
- Ach input to hypothalamus/ventral forebrain (ventral route)
- raphe nuclei
- melanin-containing hormone
What is involved in the ventral portion of the ascending arousal system?
- hypothalamus/ventral forebrain receive orexin (ORX) and melanin-containing hormone (MCH), GABA and Ach
- venterolateral preoptic nucleus (VLPO): active during sleep, contain inhibitory GABA and galanin
What is involved in the wake side of the "sleep-wake" switch?
- VLPO/eVLPO inhibited by monoaminergic nuclei thus allowing orexin to function
- orexin (ORX) stimulates LC, TMN, and raphe nuclei
- person becomes awake
What happens with damage to VLPO nuclei?
What are the basic components of the sleep and wake cycles?
- (VLPO) ventrolateral preoptic nuclei --> GABA, galanin
- pedunculopontine and laterodorsal tegmental nuclei --> Ach
- locus coeruleus --> noradrenaline
- dorsal raphe --> 5-HT
- tuberomammillary nucleus --> histamine
- basal forebrain --> Ach, GABA
- wake stabilization:
- lateral dorsal hyporhalamus --> hypocretin, orexin (ORX), melanin-containing hormone (MCH)
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