movement + thalamus (<50% have question, not priority) + basal ganglia Flashcards
reflex to test C5 nerve root
biceps
reflex to test C7 nerve root
triceps
reflex to test L4 nerve root
patellar
reflex to test S1 nerve root
achilles
dorsiflexion of large toe + fanning of other toes with plantar stimulation
+ babinksi sign (plantar reflex)
if in adults: suggests UMN lesion
let go of baby and baby abducts/extends limbs and then draws together
moro reflex
stroke cheek and baby moves head toward one side
rooting reflex
roof of mouth is touched and suck in response
sucking reflex
curling of fingers when palm is stroked
palmar reflex
baby is face down (ventral position) and stroke along one side of the spine causes lateral flexion of lower body toward stimulated side
galant reflex
what thalamic nuclei relays this information:
SENSORY signals from body (via medial lemniscus: proprioception, light touch + spinothalamic tract: pain + temp of body) → summate information to sensory somatosensory cortex
ventral posterolateral nucleus (VPL)
VPL: very painful LEGS (spinothalamic)
what thalamic nuclei relays this information:
trigeminothalamic (pain + temp of face) and taste signals → somatosensory cortex
ventral posteromedial nucleus (VPM)
VPM: very painful MOUTH (trigeminothalamic)
what thalamic nuclei relays this information:
retina (visual, CN II) → occipital lobe
lateral geniculate nucleus (LGN)
optic tracts arise from LGN
lateral: visual
what thalamic nuclei relays this information: inferior colliculus (auditory) → 1° auditory cortex
medial geniculate nucleus (MGN)
medial: auditory
what thalamic nuclei relays this information:
mammillothalamic tract → cingulate gyrus (part of Papez circuit)
anterior nucleus (part of limbic system)
what thalamic nuclei relays this information:
communications with prefrontal cortex
memory loss results if destroyed
medial dorsal nucleus
what thalamic nuclei relays this information:
cerebellum (dentate nucleus) and basal ganglia → motor cortex
ventral lateral (VL) nucleus
what thalamic nuclei relays this information:
basal ganglia → prefrontal, premotor, orbital cortices
ventral anterior nucleus
viruses and diseases that damage the anterior horn cells of LMNs
poliovirus
west nile virus
spinal muscular atrophy: werdnig-hoffmann disease
ALS (affects UMN (spasticity) + LMNs (weakness), spares sensory tracts)
deep nuclei of cerebellum ( integrates signals of cerebellum) from medial to lateral
FAST Gerbals Exercise Daily Fastigial Globose Emboliform Dentate interposed nuclei = globose + emboliform
information that helps you to maintain balance
proprioception in legs (consider if can’t stand with eyes open)
vision
vestibular apparatus (consider if can’t stand with eyes open)
romberg test
close eyes (remove visual input, can only rely on proprioception of legs (dorsal column) and vestibular apparatus)
if either damaged: fall (+ romberg test)
DOESN’T TEST CEREBELLAR FUNCTION
3° syphilis affects
dorsal columns of proprioception
+ positive rhomberg
tremor occurs at rest, disappears with voluntary movements
resting tremor
associated with Parkinson disease
resting tremor
tremor appears with voluntary movements only
intention tremor
associated with cerebellar damage (cerebrocerebllum - lateral hemisphere)
intention tremor
tremor occurs with movement and at rest
essential tremor
associated with family history of tremor
essential tremor
rapid fine tremor of head, hands, arms, and/or voice
occurs with movement + rest
50% have family history of tremor
essential tremor
treatment of essential tremor
B blocker (propranolol): DOC
primidone (anticonvulsant)
clonazepam (BZD)
alcohol (self-medicate)
lesion of substantia nigra pars compacta of basal ganglia
hypokinesis: Parkinson Disease
lesion of subthalamic nucleus of basal ganglia
hemiballismus of CONTRALATERAL extremity: lacunar stroke
neurodegenerative movement disorder
intracellular inclusion of Lewy Bodies inside neurons of substantia nigra pars compacta → lose dopaminergic neurons → can’t make dopamine
parkinson disease
depigmentation of substantia nigra
parkinson disease
lose dopaminergic neurons → not making dopamine → stop making melanin (dopa is precursor): provides pigmentation of dopaminergic neurons
neurodegenerative movement disorder
hypokinesis
bradykinesia
akinesia
postural instability
festinating gait: problem initiating walking, problem stopping so shuffle gait
resting tremor “pill rolling”
cogwheel rigidity: passively move arm and have rigidity
mask-like facies (hypokinesia of face, frozen)
parkinson disease
chemical that can cause parkinsonian features
process of synthesizing meperidine creates MPTP → metabolized to MPP → destroys dopaminergic cells in substantia nigra→ ↓ dopamine
treatment of parkinson disease
BALSA
Bromocriptine (ergot dopamine agonist), pramipexole, ropinirole (both non-ergot dopamine agonist)
Amantadine
Levodopa + carbidopa + talcapone (DOC)
Selegiline, rasagiline
Antimuscarinics (benztropine): treat rigidity, tremor (not bradykinesia)
treatment for MPTP exposure
selegiline
non-drug treatment of parkinson disease
deep brain stimulation
lesion of subthalamic nucleus →↑ movement
wild, flailing motion of unilateral arm or leg
hemiballismus
normal function of subthalamic nucleus
inhibits movement
normal function of substantia nigra pars compacta
facilitates movement
brief, purposeless, NON-repetitive jerks of individual muscles “dancing”
chorea
brief, sudden muscle contraction (like muscle spasm)
can be repetitive
myoclonus
slow, writhing, snake-like movements in hands + fingers
athetosis
compulsion (choosing) to move
akathisia: SE of some anti-psychotic drugs
AD trinucleotide repeat disorder
huntington disease
huntington disease presentation
CAG trinucleotide repeat
Chromosome Cuatro (4)
Cuarenta (40 yo)
Chorea
Cognitive decline: dementia + depression, psychosis
Caudate atrophy + putamen (part of BG called the neostriatum)
neurodegenerative disorders of BG
parkinson disease: pars compacta substantia nigra
huntington disease: caudate + putamen atrophy
excessive glutamate excitation (NMDA receptors) → kills neurons in caudate + putamen of BG
↑ dopamine: excessive movements
↓GABA: lose inhibition
↓Ach
huntington disease
treatment of huntington disease
tetrabenazine: (inhibit VMAT → block dopamine packaging + release): treat chorea
olanzapine, haloperidol (neuroleptics - dopamine antagonists): treat chorea + psychosis
normal function of globus pallidus interna
inhibit movement
