Exam 1 Quiz Flashcards
Name a presynaptic and postsynaptic acting disorder and explain how each works specifically and what each causes generally.
Pre- botulism–blocks Ach from binding the presyanptic membrane for release into synaptic cleft so nerve impulse fails to be transmitted across neuromuscular junction which causes muscle paralysis.
Post- MG– antibodies to ACh change the shape of the post synaptic membrane to be wider and have less receptors so ACh has less chance of finding a receptor to bind before it is hydrolyzed by AChesterase which causes increased muscle weakness.
Name 2 types of MG
ocular–symptoms in extraocular muscles only= diplopia and ptosis (10-15% of cases) and generalized (85%)
Where does MG weakness symptoms start?
BUE and BLE weakness starts proximal and moves distal
What is the action of recovery from botulism?
create NEW terminal nerve filaments and formation of NEW synapses at the NMJ
When using BOTOX as a tx what happens in PT?
as soon as BOTOX starts to take effect in 4-7 days PT is MANDATORY. should utilize active stretching with care to not overstretch and tear weak muscles, + reciprocal inhibition and serial casting/dynasplint if necessary AND strengthen the ANTAGONIST muscle
What kinds of pts can use BOTOX?
SCI, TBI, CVA, MS, Dystonia, hypertonicity–focal spasticity
How long does BOTOX tx last? how long until NMJ takes up? How long until see effects in pt?
3-4 months, 12 hours, 4-7 days
How does one contract botulism?
food bourne, improperly preserved foods/canned foods, wounds
Prevention for botulism?
no honey for <1 y/o, wounds clean, boil food for 10 minutes
Onset and Recovery time frame for botulism
12-36 hours for sxs, gradual full recovery in wks/months
Intervention for MG?
thymectomy(10-15% have tumor, 70% have enlargement)
anticholinesterase drugs
immunosuppressives-prednisone, cyclosporine, mycophenolate, azathioprine
IVIG
plasmaphoresis–lasts 4-6wks
Dx of MG?
Ab in blood for ACh receptors
Decremental EMG–decreased strength in repeated stimulation
Tensilon test–Achesterase inhibitor, so it acts to prevent ACh breakdown which will allow more time for it to bind to receptors= increased strength/endurance
Muscle biopsy- count ACh receptors
Symptoms of botulism
flaccid symmetrical paralysis diplopia, blurred vision, ptosis dry mouth N&V lethargy difficult swallow and speech Respiratory distress Autonomic involvement--symp/parasymp
Symptoms of MG
ocular--diplopia, ptosis=CN3 facial weakness=CN7 oropharyngeal weakness chewing/swallowing/speaking difficulty BUE/BLE weakness starts prox to dist respiratory muscle weakness Fluctuates over days/hours--better in AM, declines with day/exercise
What type of population does MG affect?
specific term needed
Bimodal–30 year old women, 60 year old men
1 in 10-20,000 in US
15-30, 60-75 y/o
females>males 3:2
What is normal in both botulism and MG?
sensory. MG also reflexes and coordination
MG crisis
respiratory or choking
Intervention for Botulism
ABE serum antitoxin, antibiotics, debridement, gastric lavage, IV, mechanical vent
example of dendritic arborization
purkinje cell in cerebellum, tree like, many inputs to 1 output for slots of integration of information
neurons–types and where seen
multipolar- motor neurons–many dendrite 1 axon
bipolar–interneuron, 1 dendrite, 1 axon
unipolar–sensory–many dendrites 1 axon, cell body is removed usually in DRG
Glial cells 4 functions
structure and support
nutrients and oxygen
myelination
destroy pathogens, remove dead cells
Glial cell types and where found
PNS-Schwann cells
CNS-oligodendrocytes, astrocytes, microglia
Schwann cell functions
myelination of 1 neuron–wraps around axon, forms nodes of Ranvier
Oligodendrocyte functions
myelination of MANY neurons
insulate and protect
increase NCV
involved in Alzheimer’s and MS
what is the most common glial cell?
astrocyte
what is the NCV of both myel/nonmyel neuron and types of each
myelinated–72-120 know 100ms, alphaMN, 12-20 diam.
unmyelinated–.5-2 know 1ms, c-sensory, chronic pain, 1-diameter
astrocytes function
fill brain space–support and insulation
maintain BBB
divide and wall off areas of damage from inflamm/injury
scavenge–remove NT’s from synaptic cleft, clean up debris in development/injury
microglia
phagocytosis!!!
protective- mobilize after injury/infect/disease
phagocytose bacteria and cells, important in devel.
destructive–in Alzheimer’s/aging=release toxins
in HIV/AIDS=cellular breakdown
how does MS tie into glial cells?
damage to myelin sheath in CNS
oligodendrocytes are attacked by own immune system Ab.
yields patches of demyelination= plaques in white matter
Where does Na and K influx/efflux occur during depolarization and what kind of conduction is it?
at the Nodes of Ranvier
Saltatory conduction
Name the 4 main symptoms of PD and how many for Dx?
other diagnostics
2/4
bradykinesia
resting tremors-pill rolling
posture instability–hypometric anticipatory adjustment
rigidity-cog-wheeling, lead pipe
can get CT or MRI to rule out other disease
positive response to DA-like medication
Name all 5 reflexes and spinal level
C5- biceps C6-brachioradialis C7-triceps L3/4-quads S1-achilles, ankle jerk, PF's
What are common causes of nerve root compression? effects?
tumor, disc protrusion, closing of facets
decreased myotome, DTR, dermatome-sensory loss, often pain
Name the myotomes and spinal level
C4- shoulder shrug C5-shoulder abduction C6-wrist extension C7- elbow extension C8-finger flexion/wrist flexion T1-abd/add of fingers L1/2-hip flexion L3/4-knee extension L5-S2-knee flexion S1/2-PF S2/3-abduction of toes
Neuro level C5
deltoid and bicep
bicep reflex
Neuro level C6
biceps, Wrist extensors(ECRL,ECRB)
brachioradialis reflex
Neuro level C7
triceps, wrist flexors, finger extensors
triceps reflex
Neuro level C8
interossei muscles
no DTR
Neuro level T1
interossei muscles
no DTR
Neuro level L4
Tib. Ant–inversion
Quad reflex
Neuro level L5
Extensor Hall. Longus
No DTR
Neuro level S1
Peroneus L and B–eversion
Achilles reflex
LMN signs and symptoms
Atrophy, weakness/paralysis, hypotonic DTRs, decreased muscle tone, fasciculations-rapid, fine, contractions of muscle fibers, painful/painless
UMN sxs
spasticity, hypo/hypertonic DTRs, clonus, +babinski/hoffman, weakness, synergistic movement patterns
Which type gives glove/sock like sensory loss
UMN
Motor loss occurs where
pre central gyrus Broadman area 4
sensory loss occurs where
post central gyrus Broadman area 3,1,2
Radial nerve
C6-8 T1
elbow extension, wrist/finger ext., supination
sensory-thumb web
Ulnar Nerve
C8 T1
interossei, little finger abd.
sensory- pinky finger
Median nerve
C6-8 T1
wrist flexion, long finger flexors, pronation
sensory- palm and tips of 1-3, 1/2 of 4th digit
Common peroneal
L4-5 S1-2
motor-DF, eversion, toe extension
sensory- lat. knee
Deep peroneal
DF, toe extension (extensors hallucis, digitorum)
sensory- between digits 1-2
superficial peroneal
Eversion (peroneus longus and brevis)
sensory- entire lat. leg
Tibial
L4-5, S1-3
Ankle PF, Inversion, toe flexion
Sensory-sole and heel
Hoehn and Yahr stages
1- unilateral, inconvient, mild, not disabling, tremor of 1 limb
2- bilateral, minimal disability, posture and gait affected
3- significant slowing of movement and QOL effect, moderately severe disability
4- Severe symptoms, rigidity, bradykin, limited ability to walk, cannot live alone
5- totally dependent-cannot stand or walk
Meds for parkinsons and how they work
Medication–L-dopa-breaks down b4 BBB-1% effective, sinemet–perfect design, decreases brady and rigid–other side effects though, ropinorole, pramipexole, neupro patch-last 3 cross BBB to stimulate DA receptors directly=less dyskinesia
DELICATE BALANCE/ON/OFF phenomenon/DRUG HOLIDAY
Surgery for PD and how\/why better
DBS-deep brain stimulation
reversible, better for bilateral, fewer side effects, less severe fluctuations and amplitude, stim of GP or STN= decrease of all symptoms and decrease of dyskinesia
Stereotaxic- ablate a part of BG–GP-palladotomy=decrease brady, tremor, rigid. OR thalamotomy= decrease tremor
PD–how much decrease in neurons or DA b4 sxs?
80% for both
Other PD tx?
external sensory cues–laser cane–visual cue for floor, music therapy-pulse or beat…Dr. Ed Roth
What types of BG disorders and who is in what one?
Hypokinetic-PD
Hyperkinetic-Huntington’s chorea, Dystonia, Tourette’s
What is effected in PD BG?
The SNc is degenerated so it does not make enough DA and the thalamus is over-inhibited which leads to under-facilitation of cortex.
What is effected in Huntington’s chorea?
The striatal neurons to SNr and LGP are degenerated. which leads to under-inhibition of the thalamus and over-facilitation of the cortex
What is effected in Tourette’s?
disturbance in limbic system circuits causes inhibition of SNc= less inhibition of thalamus, over-facilitation of cortex
What is effected in Dystonia?
unknown etiology–usually from vascular issue–stroke, TBI, anoxia
can be genetic–general dystonia–DYT1 gene–onset 8y/o
can be lesions of any/all BG–focal dystonia–affects 1 body part/joint/related joints, onset at 30-50y/o
PD sxs
difficulty swallowing/chewing
speech impaired–too soft, monotone, hesitant, slurred
flat affect of face
fatigue, sleep problems
decreased strength of respiratory muscles
dimentia/cognitive problems
kyphosis, flexed trunk, forward head, crouched legs
micrographia-words are cramped and slow
Difficulty initiating GAIT-freezing, festinating–shuffle/fall
decreased trunk rotation and arm swing
Death in PD
usually choking, pneumonia, falls after ~20 yrs
Death in Huntington’s
15-20 years after onset, probably from choking, weight loss
Death in Freiderich’s ataxia
HEART DISEASE/ATTACK
Onset for PD..How?
idiopathic-unknown
MPTP
How does Sinemet work?
carbidopa prevents levodopa from being broken down b4 it crosses the BBB, but carbidopa cannot cross too so L-dopa gets to breakdown once inside the brain.
lasts 4-5 years before tolerance generated.–2 thoughts: save for later, or use now b4 too few neurons in SNc
Dystonia sxs
simultaneous contraction of agonist and antagonist muscle–sustained contraction at end ROM–involuntary
can be rapid or slow, rhythmic or unpatterned
can last minutes to hours +
rigidity, usually painful, contorted/twisted postures
can be onset by stress, purposeful mvmt, task-specific activity–musicians or writers
NOT FATAL- decreased with relax and sleep
Tx for Dystonia?
BOTOX for focal
General-baclofen, artane, sinemet, klonopin
DBS of GP, or Rhizotomy
Dystonia types
focal–pharyngeal, cervical–most common–not torticollis, writers cramp, musicians cramp–progresses for ~5 years–30% spontaneous recovery
General- entire body-genetic
begins in legs and progresses to rest of body. starts with a mvmt then twisted trunk, then to UE, LE
Tourettes sxs
impulsions/compulsions to perform fragments of motor programs
TICS- skipping, jumping, touching, vocalization
Huntington’s sxs
Aspects of behavioral, cognitive, and motor chorea-invol small amplitude, rapid mvmt akinesia/bradykinesia hypotonia wide, staggering gait speech lacks timing and rhythm difficulty swallowing saccadic eye mvmts dementia, poor judgement, decreased long term memory, depression and irritability
Huntington’s onset
after ~30 y/o death 15-20 years later. Mauritius has high population 1 in 2,166
HC Early stage
symptoms for DX–can continue work/drive/etc.
starts in EXTREMITIES–invol twitches of fingers/toes/face
subtle loss of coordination
harder to work and perform at usual cog level
difficult to think through complex tasks
depression, irritability, DISINHIBITION
HC middle stage
loss of ability to work and drive
difficulty swallowing, slurred speech, staggering walk, CHOREA, weight loss
difficulty thinking clearly, organizing info, problem solving
increased APATHY, loss of interest in activities and increased depression, irritable, disinhibited more
HC late stage
totally dependent, bed ridden, unable to speak, choke, tube fed
severe rigidity, dystonia, bradykin. Chorea usually gone
cannot initiate mvmt
cognitively debilitating–recognize faces, understand speech
depression fades, increased apathy, psychosis in some
HC medication
cholinergic-GABA containing perphenazine haloperidol reserpine riluzole
unified HD rating scale UHDRS
motor assess cog assess behavioral assess independence scale functional scale total functional capacity
parts of a neuron…go
dendrite, cell body, axon hillock, axon, node of ranvier, myelin sheath, presynaptic terminal, presynaptic membrane, synaptic cleft, post synaptic membrane
functions of both neo and spino
comparator–compares actual outcome to intended motor program.
collects continuous info about desired program from M1, PMA, SMA cerebral cortex
collects continuous info from peripheral muscle spindles, GTO’s, proprioceptors, and tactile receptors about instant status of body–body parts, position, force, and rate of motion
How much time does it take to correct an action in the moment?
100-200ms
functions of both vestibulo and spino
excitatory influence on gamma motor neurons
with acute cerebellar damage, decreased excitation of gamma’s=decreased sensitivity of spindles=decreased tone-hypotonicity
what part of brain contains more neurons than anywher?
Cerebellum
8 cell types in cerebellum
Purkinje, Granule, Golgi, Parallel, Stellate, Basket, Mossy fibers, Climbing fibers-afferent input
4 types of deep nuclei
fastigial
interposed-globose and emoliform
vestibular–flocculonodular
dentate-worm like
Where are all the axons to/from cerebellum held?
in the peduncles
Main function of cerebellum and how it does its job
vast integration of info concerning mvmt and complex computations of movement,
because of the infolding-gyri and sulci–all anatomically similar
Vestibulocerebellum inputs and what they are bringing in
from vestibular nuclei to the focculonodular lobe
sense change in linear/angular head position, rotation, accel/deceleration
Vestibulocerebellum outputs and function
from flocculonodular to vestibular nuclei
coordinates eye/head mvmt, equilibrium and balance, coordinates proximal musculature of axial body–head, neck, trunk, pelvis/hips, scap/shoulder
senses rapid position and direction changes
Neocerebellum inputs and where
from ipsilateral cortex, to corticopontocerebellar tract to pontine nuclei to LATERAL ZONES–frontal and parietal lobe, motor, sensory, PMa, SMA
Neocerebellar outputs
dentate nucleus to VL thalamus, to premotor and motor cortices
Neocerebellar function
planning and timing of voluntary movements, particularly learned, skillful movement that becomes more rapid, precise, and automatic with practice
motor planning of sequential movement
onset, rate, amplitude, and duration of agonist and antagonist mm.
SO= associated with mvmt DECOMPOSITION, and DYSMETRIA
Spinocerebellar inputs to vermis and what
dorsal spinocerebellar, cuneocerebellar, and trigeminocerebellar from head and trunk
Also, vestibular and tectocerebellar–from superior-visual and inferior-auditory- colliculi
Spinocerebellar inputs to intermediate zone and what
dorsal spinocerebellar, cuneocerebellar from UE and LE
Spinocerebellar outputs from vermis
GROUP A-GROSS MOTOR
thalamus->M1 area->Anterior CST
fastigial nuclei->reticular nuclei->CMRST
vestibular nuclei->vestibulospinal tract lat and med.
Spinocerebellar outputs from intermediate zone
GROUP B-FINE MOTOR
thalamus->M1 area and SMA->Lateral CST
reticular nuclei->CPRST
interposed nuclei->red nuclei->rubrospinal tract
Spinocerebellar function from vermis
GROSS MOTOR MVMT
coordination of axial and girdle musculature
regulates rhythmic walking–CPG’s of gait
adjusts timing of locomotor mvmt
interlimb coordination
Spinocerebellar function from intermediate zones
FINE MOTOR MVMT
coordination of distal musculature of distal extremities, hands and feet
Name the lobes and zones of cerebellum
anterior lobe, posterior lobe, flocculonodular lobe
vermis, intermediate zone, lateral zones
What will happen with damage to cerebellum?
poor coordination without overt muscle weakness
Hypotonicity
decreased firmness and tone during PROM, pendular DTR’s, decreased extensor tone=trouble remaining upright
Asthenia
general weakness or decreased activity and easy fatigue
intention tremors and amplitude
3-5 Hz, amplitude increases as effector approaches target
disturbances of posture and balance
flexed posture, wide BOS, poor equilibrium and balance especially in axial body and rapid changes
VESTIBULOCEREBELLUM
Dysmetria
over or under shooting, left or right,up or down
past-pointing
force issue—triphasic EMG–AG1, ANTAG and AG2 not programmed correctly
NEOCEREBELLUM
Dysdiadochokinesia
rapid alternating supination/pronation
shin test
deficit in coordination–errors in rate/timing, range/amplitude
Ataxic gait
disruption in rhythm of gait, wide based gait, unsteady
falls are back and toward side of lesion
SPINO-VERMIS
Movement Decomposition
disruption in sequence in a multi step task, breaking a multi-joint movement into a series of seperate movements
NEOCEREBELLUM
Poor coordination of muscles associated with speech
dysarthria-slurred
explosive/staccato speech
Eye movements
gaze evoked nystagmus, ocular dysmetria, disrupted smooth pursuit, poor coordination of eye/head movement.
VESTIBULOCEREBELLUM maybe more
TIme asymetric velocity profiles
normal=equal time in accel./decel.
mild= more time in decel.
severe= more time in accel.
Delays in force production and error in force maintenance
difficulty generating enough force, matching to the wt. of the object, and maintaining that force
Friederich’s ataxia onset
hereditary, 5-15 y/o, 25% of offspring
lesions affect cerebellum
DRG-sensory
dorsal columns-conc. prop., fine touch, vibration
spinocerebellar tracts-unconcious proprioception
some corticospinal tract involvement
Friederich’s ataxia sxs
ataxia of gait 1st then extremities clumsiness, intention tremor loss of extrem sensation \+babinski decreased DTRs tone is normal at rest nystagmus and impaired smooth pursuit HEART DISEASE easily fatigued scoliosis slurred difficult speech
FA life expectancy
60-70 if no Heart attack
progressive disease where you eventually lose ability to walk and confined to wheelchair in 10-20 years
Cerebellar stroke
less than 5% of all strokes involve Post/inf, Ant/inf, or superior cerebellar arteries
if deep cerebellar nuclei are involved->px worse
Cerebellar tumor
Children more common but have better PX b/c usually benign and removed with surgery
Adults–more likely aggresive cancer–poor Px
Static balance T
maintain a position over time–time is the measure
Static balance R
maintain a position against resistance
rhythmic stabilization and alternating isometrics
Static Balance AFF
maintain a position while reaching within arms length
Anticipatory feed forward
Dynamic Balance RFB
reactive feedback
sitting/standing–manually place COM to edges of BOS to elicit an equilibrium reaction–movement of trunk, arms, legs to counteract the balance point
Dynamic Balance AFF
anticipatory feed forward
sitting/standing–reach in various directions beyond arms length to elicit various trunk and arm balance reactions
Protective reactions
slow/quick displacement of COM outside BOS to elicit a change–placing a hand or foot out to catch the body
Functional balance
AFF and RFB –utilizing effective balance strategies while performing a set of functional tasks that increases in difficulty
