Exam 2 Flashcards
where are the cell bodies of LMNs located?
in the ventral horn of the SC
are LMN peripheral neurons?
yes!
what are the signs of a LMN lesion?
hypotonicity
hyporeflexia/areflexia
neurogenic atrophy
fasciculation/fibrillation
paralysis and paresis
do UMNs or LMNs lesions result in neurogenic atrophy?
LMN lesions
do UMN or LMN lesions result in disuse atrophy?
UMN lesions
what is hypotonicity?
low muscle tone (abnormally low resistance to passive motion)
what is muscle tone?
resistance to muscle stretch in resting muscle
what is flacidity?
more severe where there is an absence of resistance to passive movement
do UMN or LMN lesions result in resting tension close to none?
LMN lesions
why can hypotonicity lead to injury?
there is ligament laxity and hypermobility of the jts
lack of voluntary muscle control
what is the importance of the phasic stretch reflex/DTR?
it determines the integrity of the monosynaptic reflex and SC at different segmental levels
it determines the excitability of the alpha motor pool
is phasic stretch reflex the same thing as tonic stretch reflex?
no! tonic stretch reflex is abnormal
what does diminished input from motor neurons to skeletal muscles lead to?
hyporeflexia
what is neurogenic muscle atrophy?
rapid loss of muscles bulk due to denervation of skeletal muscle associated with LMN lesions
what chain of events lead to neurogenic atrophy?
lack of neural stimulation and contraction–>lack of gene expression–> changed protein production–>rapid atrophy
what is this describing?: a ground motor neuron is trying to innervate a lot of motor fibers but can’t support them so they die
neurogenic atrophy
what is fasciculation?
spontaneous quick twitch of a single motor unit (one motor neuron and all its fibers it innervates) that can be seen
not always pathological like an eyelid twitch
is a fasciculation pathological?
not always
when is fasciculation pathological?
with atrophy
what are some common causes of fasciculation?
too much caffeine
fatigue
what is fibrillation?
spontaneous contraction of muscle fibers that can’t be observed with the eye
pathological sign of denervation/electrolyte imbalance
what is fibrillation a sign of?
denervation
electrolyte imbalance
is fibrillation pathological?
yes!
what causes fibrillation?
muscles not getting enough ACh, so the receptors get dispersed and become hypersensitive to ACh
what is paralysis?
completely severed nerve with no way of getting signals to the muscles
is paralysis or paresis more common in LMN lesions?
paralysis
what is paresis?
cut a few nerve fibers w/remaining fibers leads to weaker muscles but not completely paralyzed
how are paralysis and paresis measured?
MMT and dynamometer
are these examples of UMN or LMN disorders?:
poliomyelitis
GBS
Erb’s palsy
Klumke’s palsy
myasthenia gravis (not really though)
LMN
what is poliomyelitis?
polio virus selectively destroys somas of MNs leading to denervation of muscle fibers and weakness of muscles
do poliomyelitis effect one or both limbs?
one limb
do the impairment of poliomyelitis last a lifetime?
yes:(
can there be some recovery in poliomyelitis? why or why not?
yes, bc it is PNS
is poliomyelitis worse in children or adults?
adults, it will result in quadriplegia
who is mostly effected by poliomyelitis?
children under 5 y/o
doe poliomyelitis have mostly motor or sensory symptoms?
mostly motor
what is post-polio syndrome?
overextension of surviving MN following poliomyelitis results in death of neurons that tried to take on orphan fibers
occurs years after initial viral infection
what are the s/s of post-polio syndrome?
increasing weakness
fatigue
jt and muscle pain from muscles fatigue (achy)
breathing difficulty
t/f: the s/s of the initial infection correlate to the severity of the post-polio symptoms
true
t/f: pts with post-polio syndrome are a fall risk
true
what is Erb’s palsy?
brachial plexus injury from birth trauma or falling in neck lateral flexion resulting in avulsion of C5-6 nerve roots
motor and sensory symptoms
arm paralysis
medial rotation or the shoulder, elbow extension, and wrist flexion
what is the pattern of sensory loss in Erb’s palsy?
dermatomal
what is the pattern of motor loss in Erb’s palsy?
myotomal
what LMN disorder results in the “waiter’s tip” deformity?
Erb’s palsy
what is the prognosis for Erb’s palsy?
usually pretty good but depends on severity of the initial injury
if a pt with Erb’s palsy makes a recovery when would this recovery occur?
about 9 months after birth
what is Klumpke’s palsy?
a brachial plexus injury from traction of an abducted arm that results in avulsion of C8-T1 nerve roots
sensory and motor loss
severe pain in the nerve path
atrophy of hand muscles
hyperextended MCP jts, flexion of PIP and DIP jts (intrinsic plus)
paralysis of intrinsic hand muscles, wrist flexors, and finger flexors/extensors
what LMN disorder results in the “claw hand” deformity?
Klumpke’s palsy
what are the UMN tracts?
lat/med corticospinal, lat/med vestibulospinal, reticulospinal, and rubrospinal tracts
what does the lat corticospinal tract control?
fractionated movement for fine object manipulation
what does the med corticospinal tract control?
posture
what UMN tracts come from the BS?
vestibulospinals, reticulospinal, and rubrospinal tracts
are the basal ganglia and cerebellum UMNs?
no!
what is the corticobulbar (cortico-brainstem) tract?
from the primary motor cortex to the CN nuclei in the BS decussation at different levels
controls muscles of the face, tongue, and neck (pharynx and larynx)
describe the innervation of the upper face
innervated by 2 UMNs
contralateral and ipsilateral innervation
redundancy bc it’s innervated by both sides of the cortex
describe the innervation of the lower face
contralateral innervation only
no redundancy=no compensation with damage to one side
what are the non-specific motor tracts?
emotional motor system
what activates the emotional motor system?
excessive limbic activity
t/f: there is poorer motor performance with high anxiety
true
how does the emotional motor system control movement?
modulates the activity of interneurons and LMNs
what is the ceruleospinal tract?
fast acting system
NE=induce sympathetic activity
slightly depolarized LMN makes it easier to excite
adrenaline in antinociception that suppresses pain perception
what is the raphespinal tract?
serotonin
modulation of LMNs
what are the signs of UMN lesions?
hypertonicity
disuse atrophy
abnormal reflexes
abnormal synergies
movement disturbances
impaired postural control
what is disuse atrophy?
slower progression of atrophy due to lack of muscle use
more mild than neurogenic atrophy
is paresis or paralysis more common in UMN lesions?
paresis
what is hypertonicity?
abnormally strong resistance to passive stretch
neuromuscular overactivity and excessive contraction from an UMN lesion
what are the 2 types of hypertonicity?
spasticity and rigidity
what is spasticity?
velocity-dependent increase in resistance to stretch
increased velocity=increased hypertonicity
should you move a limb slower or faster to avoid spasticity?
slower
what are the 2 mechanisms of spasticity?
1) hyperreflexia at the level of the SC
2) BS motor tracts overactivity
t/f: muscles shorten secondary to spasticity
true
what is rigidity?
velocity independent increase in resistance to stretch
constant resistance to passive movement regardless of the speed of the force applied
BS lesions above the red nucleus- produce what?
decorticate posture
what is the decorticate posture?
“arms to the core”
red nucleus- no longer under cortical inhibition=UE flexion
what is decerebrate posture?
results from lesion below the red nucleus but above the vestibular nuclei
no rubrospinal contribution for UE flexion=UE extension
vestibular nuclei no longer under cortical inhibition=UE extension
what is a common feature of both decorticate and decerebrate posture?
necks and trunk extension
typically in response to noxious stimulus (sternal rub)
what is reflex irradiation?
reflex test performed on one area results in reflex of another adjacent area
ie: reflect test of quad tendon results in hamstring and quad reflexes
ie: one side tendon tap results in rxn on both sides
what are signs of corticospinal tract (CST) damage (UMN)?
positive Babinski sign
positive Hoffman sign
what is a positive Babinski sign?
toes fan out w/stroking of the lateral plantar side of the foot
what is a positive Hoffman sign?
opposition of the thumb and index finger when the examiner flicks the nail of the middle finger down
what is clonus?
involuntary, repeating, rhythmic contractions of a single muscle group induced by muscle stretch, noxious stimulus, or voluntary movement
where is clonus commonly seen?
at the ankle
what injury commonly results in clonus?
SCI
what is the clasp knife response?
with slow stretch of paretic muscle, resistance is initially strong and sudden goes away
what is the result of a lesion in the corticospinal tract?
disinhibition of the reticulospinal tract
abnormal synergy patterns
loss of fractionation of movement
what is fractionated movement?
ability to isolate one jt movement from another
what is abnormal UE flexion synergy?
scap retraction, elevation or hyperextension
shoulder abduction and external rotation
forearm supination
wrist and fingers flexion
elbow flexion*
what is abnormal UE extension synergy?
scap protraction
shoulder adduction*, internal rotation
forearm pronation
wrist and fingers flexion
elbow extension
what is abnormal LE flexion synergy?
hip flexion*, abduction, and external rotation
knee flexion
ankle dorsiflexion
toe flexion
what is abnormal LE extension synergy?
hip extension, abduction*, and internal rotation
knee extension*
ankle plantarflexion* and inversion
toe extension
what are the pathological reflexes of UMN lesions?
(+) Babinski sign
(+) Hoffman sign
reflex irradiation
clasp knife response
what are the pathological reflexes of LMN lesions?
absent reflexes
what are the UMN disorders?
spina bifida
Arnold chairi malformation
MS
cerebral palsy
stroke
SCI
trauma (TBI)
tumor
what is the most frequently affected artery in strokes?
middle cerebral artery
what the pathology of a stroke?
interruption in blood flow to the cerebrum
what tracts are effected by stroke?
corticospinal tracts
corticoreticular tract
corticobrainstem tracts
what are the impairments in stroke?
contralateral motor impairments
contralateral sensory impairments: all face and body modalities
contralateral UMN signs
where do the upper and lower face get innervation from?
corticobulbar tract
if there is a lesion to the cortiobrainstem tract, what is the pattern of loss in the face?
UMN
paralysis of the contralateral lower face
if there is a lesion to the facial nerve(CN), what is the pattern of loss in the face?
LMN
no motor function on one side of the face
t/f: the raphespinal and ceruleospinal tracts may be able to produce a smile in the paralyzes lower side of the face with a corticobulbar tract lesion
true
is ALS an UMN or LMN disorder?
both
what is amyotrophic lateral sclerosis (ALS)?
selective destruction of motor neurons (LMN) and motor pathways (UMN) causes gradual onset of progressive muscle weakness
is ALS usually idiopathic?
yes
when is ALS usually diagnosed?
age 40-70
what is the life expectancy of someone after an ALS diagnosis?
2-5 years
are there sensory impairments in ALS?
no
how is ALS different from SMA?
SMA involves lack of SMN gene that leads to death of neurons and is solely LMN
ALS is both UMN and LMN
what are the UMN signs associated with ALS?
(+) Babinski sign
increased DTR
slow/rapid alternating movements
what are the UMN symptoms associated with ALS?
lack of movement coordination
poor balance
stiffness w/UE and LE movements
what the LMN signs associated with ALS?
difficulty squatting and rising from a chair
foot drop
UE and LE atrophy
waddling gait
fasciculations
what are the LMN symptoms associated with ALS?
muscle cramps
fasciculations
UE and LE weakness
what are the disorders of the ANS?
Horner’s syndrome
orthostatic hypotension
syncope
autonomic dysreflexia
diabetic autonomic neuropathy
what is the central autonomic pathway?
the hypothalamospinal tract
what is the dysfunction associated with a hypothalamic lesion?
metabolic (impaired thermoregulation, obesity, anorexia) and behavior dysfunction
what is the dysfunction associated with a limbic lesion?
altered autonomic responses to emotion (no longer have sympathetic responses paired with emotional responses)
what is the dysfunction associated with a brainstem lesion?
loss of descending control of HR, BP, and respiration
autonomic dysfunction associated with CN damage (pupillary control, swallowing, salivation, tear production)
what is the dysfunction associated with SC lesions?
loss of ascending and descending autonomic signals at and below the lesion
vasomotor, HR control, etc affected (autonomic dysreflexia)
what is the dysfunction associated with peripheral nerve lesions?
loss of vasomotor control, temp regulation, and sweating bc peripheral nerve contain autonomic fibers
trophic changes (changes in skin elasticity) affecting hair and nail formation-blotchy, red, cyanotic, thin, cold, or hot skin
what is Horner’s syndrome?
PAM due interruption of sympathetic efferent pathway (hypothalamospinal/brainstem tracts) affecting the ipsilateral face
what does PAM stand for in Horner’s syndrome?
Ptosis (drooping eyelid)
Anhidrosis (loss of sweating)
Miosis (constricted pupil)
why is the pupil contracted in Horner’s syndrome?
it is a parasympathetic function from no opposing sympathetic force
in Horner’s syndrome, the pupil is >__% smaller than the other side
50
why do people with Horner’s syndrome have dry red skin?
vasodilation (parasympathetic function)
what are the causes of Horner’s syndrome?
tumor, stroke, trauma, disease affecting area surrounding sympathetic nerve, genetics
what is orthostatic hypotension?
decrease of greater than or equal to 20 mmHg SBP or 10 mmHg DBP or HR increase of more than 20 bpm during the 1st 3 minutes of standing
what is the pathology of orthostatic hypotension?
impaired reflex mediated by the arterial baroreceptors that normal constrict vessels when standing
what are the s/s of orthostatic hypotension?
dizziness, light-headedness, feeling faint, fainting
can orthostatic hypotension be neurogenic?
yes
what are neurologic causes of orthostatic hypotension?
SCI
peripheral neuropathy
autonomic degenerative disorders (Parkinson’s)
what is postural orthostatic tachycardia syndrome (POTS)?
HR increase of greater or equal to 30 bpm within initial 10 minutes of standing
absence of orthostatic hypotension and other explanations tachycardia
t/f: POTS is caused by anxiety/psychological factors
false
what population is frequently affected by POTS?
females 15-50 y/o
what are causes of POTS (other than prolonged bed rest)?
trauma, sympathetic NS overactivity, low blood volume, cardiogenic deconditioning
what is syncope?
fainting-temporary loss of consciousness bc of inadequate blood flow to the brain
decreased BP and HR
recovery w/o intervention or lingering symptoms
what is neurocardiogenic syncope?
caused by emotional response
ie. when seeing a needle or lots of blood, getting excited or shocking news
vasovagal syncope
what is situational syncope?
caused by mechanoreceptor activation on CNs
cough, sneeze, defecation, urination
what is carotid sinus sensitivity syncope?
caused by pressure on the carotid artery
ie. turning head, tight collar
what are causes for syncope?
mechanoreceptors triggered to slow the HR
medulla inhibits the sympathetic NS-signal to the vagus nerve
what is autonomic dysreflexia?
sympathetic overactivity in pts with SCI at/above T6 level
dangerous vasomotor response to noxious stimuli below the level of injury
pain below the lesion can’t be felt and triggers a sympathetic response below the lesion that can’t reach above the lesion and parasympathetic response above the lesion that can’t get below the lesion
decreased HR above the lesion
dissociated sympathetic/parasympathetic activity
what are the s/s of autonomic dysreflexia?
HTN, bradycardia, excessive sweating above the lesion, flushing of the face, pounding headache
should you lay down a pt if you suspect that they have autonomic dysreflexia?
NO! THIS WILL KILL THEM BY SENDING MORE BLOOD UP TO THE HEART
what is diabetic autonomic neuropathy?
damage to the PNS including sympathetic nerves
what are the s/s of diabetic autonomic neuropathy?
increased sweating in the extremities
trophic changes in the distribution of the peripheral nerve (shiny, hairless, anhidrosis of the skin)
postural (orthostatic) hypotension bc there is a lack of vasoconstriction in the legs bc of loss of sympathetic fxn
decreased ANS fxn following the glove and stocking pattern
impaired motility of the GI tract, gallbladder dysfunction, diarrhea, b/b dysfunction, impotence
what are the functions of the cerebellum?
movement coordination
feedback/feedforward
comparator
what does cerebellar dysfunction affect?
posture, automatic movements, eye movements, and voluntary movements
a unilateral lesion of the cerebellum will affect what side of the body?
ipsilateral bc most pathways projecting from the cerebellum stay ipsilateral or double decussate
what is spinocerebellar ataxia?
poor hand-eye coordination, poor eye movement, poor balance, poor coordination, and poor speech
what does vestibulocerebellar lesion result in?
unsteadiness
truncal ataxia
nystagmus
vertigo
what is the input of the vestibulocerebellum?
vestibular apparatus
what is the output of the vestibulocerebellum?
vestibular nuclei controlling eye movement and balance/equilibrium
what is the nucleus associated with the vestibulocerebellum?
the fastigial nucleus
what region of the cerebellum is the vestibulocerebellum in?
fluculonodular lobe
what region of the cerebellum is the spinocerebellum in?
vermis and paravermis-
what region of the cerebellum is the cerebrocerebellum in?
the lateral hemispheres
what is the input of the spinocerebellum?
visual, auditory, and vestibular inputs
what is the output of the spinocerebellum?
lateral UMNs
what does a lesion in the spinocerebellu result in?
truncal ataxia
limb ataxia (dysdiadochokinesia and dysmetria)
ataxic gait
intention tremor
dysarthria
movement decomposition
what is dysdiadochokinesia?
the inability to make rapid alternating movements like fast pronation/supination
what is dysmetria?
inability to measure distance of movement, so there is often overshooting and undershooting of targets
how is dysmetria tested?
nose to finger test
what is ataxic gait?
wide BOS and instability results from truncal or limb ataxa
what is an intention tremor?
tremor during movement (cerebellar sign)
what is dysarthria?
slurred speech
what is movement decomposition?
segmental movements can’t happens in one motion
what is the input of the cerebrocerebellum?
cerebral cortex
what is the output of the cerebrocerebellum?
motor and premotor cortex
what does a lesion in the cerebrocerebellum result in?
finger ataxia
dysarthria
what is the nucleus associated with the spinocerebellum?
interposed nucleus
what is the nucleus associated with the cerebrocerebellum?
dentate nucleus
is the paravermis lateral or medial motor?
lateral
is the vermis lateral or medial motor?
medial
does the use of vision change gait performance with cerebellar ataxia?
no
will sensory or cerebellar ataxia have a positive Romberg test?
sensory?
t/f: cerebellar ataxia limits timing and accuracy of voluntary motor control
true
what are the characteristics of cerebellar ataxia?
delayed, jerky movement
range of movement errors (longer to get from nose to finger)
patterned movement errors (dysdiadochokinesia)
truncal ataxia
gait and limb ataxia
hand and finger ataxia
what is spinocerebellar atrophy?
an inherited, neurodegenerative, heterogeneous disease subset of cerebellar ataxia
progressive degeneration of the cerebellum caused by CAG nucleotide abnormally repeating expansion that encode polyglutamine
what is ACDA 1?
cerebellar ataxia
pyramidal features
extra pyramidal features
amytrophy
what is ACDA 2?
cerebellar ataxia
pigmentary retinal degeneration
what is ACDA 3?
pure cerebellar ataxia symptoms
what are the signs of spinocerebellar atrophy?
dystonia
muscles fasciculations
poor hand-eye coordination
slurred speech
learning disabilities
parkinsonism
hyperreflexia
seizures
what are the symptoms of spinocerebellar atrophy?
difficulty walking
reduced b/b control
involuntary eye movements
difficulty swallowing
muscles weakness, stiffness, and cramps
numbness
how is spinocerebellar atrophy diagnosed?
genetic testing
neuro imaging
electrophysiologic testing
is there a cure for spinocerebellar atrophy?
no:(
what meds can be used to manage spinocerebellar atrophy?
antiepileptic drugs
Botox
beta-blockers
primidone
antidepressants
Levodopa
dantrolene
antisense oligonucleotides
what are activity limitations in spinocerebellar atrophy?
decreased walking distance and stability
decreased cognition
impaired balance w/surface change and in static posture
what are participation restrictions in spinocerebellar atrophy?
difficulty w/ambulation and balance for ADLs
withdrawal from social situations
work
t/f: PT can delay the need for a WC in spinocerebellar atrophy
true!
what can PT do for a pt with spinocerebellar atrophy?
exercise and balance based therapy to improve motor fxn
accessory respiratory muscles strengthening and diaphragmatic breathing exercises to improve respiratory fxn
what are the hypokinetic disorders?
Parkinson’s disease
atypical parkinsonism
what are the hyperkinetic disorders?
Huntington’s disease
dystonia
what are the disorders of the basal ganglia?
hyperkinetic diseases (Huntingtons and dytonia)
hypokinetic diseases (Parkinson’s, and parkinsonism)
basal ganglia stroke
what is hypokinesia?
less movement
hypokinesia results from down regulation of the ___ pathway and up regulation of the ____ and ___ pathways
go, no-go, stop
hyperkinesia results from up regulation of the ____ pathway and down regulation of the ____ and ____ pathways
go, no-go, stop
what are the 2 types of hypokinesia?
bradykinesia and akinesia
what is bradykinesia?
slow movement (decreased velocity of movement)
what is akinesia?
lack of movement (decreased amount of movement)
what is dyskinesia?
uncontrolled, irregular, involuntary movement
what is cogwheel rigidity?
intermittent break in tone
on and off rigidity
what lead pipe rigidity?
resistance throughout
what is the pathology of Parkinson’s disease (PD)?
idiopathic neurdegenerative disease that causes loss of dopaminergic neurons in the SNpc
when does the onset of PD usually begin?
50-60 y/o
t/f: men are more affected by PD
false, men and women are affected equally
there are no s/s of PD until __% of dopaminergic neurons are dead
80
what is the most common type of PD?
postural instability gait difficulty PD (50%)
what are the 3 types of PD?
postural instability gait difficulty PD
tremor dominant PD
mixed type PD
what happens to the GPi in PD?
it becomes more inhibitory
what is the result of the GPi becoming more inhibitory in PD?
the motor thalamus, PPN, and MLR are always inhibited
what is the result of the lack of motor thalamus activation from increased inhibition from the GPi
bradykinesia and hypokinesia
what is the result of the lack of PPN activation from increased inhibition from the GPi?
trunk rigidity
what is the result of lack of MLR activation from increased inhibition from the GPi?
changes in gait
what are the characteristics of gait in PD?
festinating, freezing gait
hard to start and once started it speeds up
sudden stopping
what are the cardinal signs of PD?
TRAP:
resting Tremors
Rigidity
Akinesia
Postural instability gait deviations
what are resting tremors?
a basal ganglia sign
tremor when not doing anything
usually a “pill rolling” tremor
what is akathisia?
restless feeling
feel like they have to move
can’t stay still
may be the first sign of PD way b4 other signs and dx
what are postural instability gait deviations?
shuffling gait
decreased arm swing and trunk rotation
retropulsion
stopped posture
poor anticipatory and reactive postural responses
what is retropulsion?
a tendency to fall or walk backwards with a a slight push back
what are the non-motor manifestations of PD?
impaired autonomic fxn
insomnia/daytime somnolence
depression
bradyphrenia
difficulty shifting attention
dementia
dysphoria
apathy and psychosis
visuospatial/visuoperceptual impairments
why is there impaired autonomic fxn in PD?
there’s inadequate NE released leading to thermoregulation dysfunction and neurogenic orthostatic hypotension
why is there insomnia in PD?
disruption of RAS and circadian rhythm
t/f: insomnia in PD can contribute to depression
true
t/f: depression in PD can be neurogenic or situational
true
what is bradyphrenia?
pathological slowing of cognitive processing
what is dysphoria?
profound feeling of unhappiness, discomfort, and dissatisfaction towards everything
what are the secondary neurologic impairments in PD?
impaired communication
masked face (hypomimia-lack of facial expression)
hypokinetic dysarthria (impaired speech) and hypophonia
what are secondary impairments of PD?
neurologic impairments
impaired oral motor control
impaired fine and gross motor performance
impaired motor learning and planning
what are the secondary oral impairments in PD?
dysphagia (difficulty swallowing)
sidlorrhea (drooling/excessive salivation)
what is a secondary fine and gross motor impairment in PD?
micrographia (small writing)
how can PD be managed?
medications and surgery
what medications are used to manage PD?
dopamine replacement
what surgeries can treat PD?
deep brain stimulation and destructive surgery
what does deep brain stimulation do in PD?
an electrode goes to the thalamus to activate it
what does destructive surgery do in PD?
destroys the GP to reduce bradykinesia and rigidity
what are the additional s/s of atypical parkinsonism?
rapid disease progression
signs of cerebellar and corticospinal dysfunction
early postural instability and retropulsion
voluntary gaze dysfunction (supranuclear gaze palsy)
respiratory dysfunction
pseudo-bulbar affect (PBA)
what is PBA?
uncontrollable/inappropriate emotions
laughing or crying out of context
what causes PBA?
disinhibition of pathways involving serotonin and/or glutamate
disconnect b/w frontal lobe controlling emotions and cerebellum where emotions are mediated
does parkinsonism respond well PD meds?
no
what is multiple system atrophy (MSA) and its key impairements?
progressive disease involving cerebellar signs, CST dysfunction, autonomic dysfunction, cardiac issues, and decreased sweating
what are other s/s of MSA?
generalized weakness, double vision/visual disturbances, difficulty breathing and swallowing, and sleep disturbances
what s/s can set apart PD and MSA?
generalized weakness as this is usually present in MSA but is not common in PD
what is progressive supranuclear palsy (PSP)?
abnormal eye movements with early onset gait instability, freezing gait, axial rigidity, dysarthria, and dysphasia
due to the buildup of tau proteins (like Alzheimer’s)
when does PSP usually begin?
age 60-70
what is a risk factor for PSP?
age
what is dementia with Lewy bodies?
an abnormal accumulation of Lewy bodies inside nuclei of neurons in the brain areas that control motor control and cognition
what are the s/s of dementia with Lewy bodies?
parkinsonism motor symptoms
early progressive cognitive decline
fluctuations in alertness and attention
visual hallucinations
depression
what is corticobasal syndrome?
assymetric involuntary movements, apraxia, and cortical sensory deficits that begin in 60s with a life expectancy of 6-8 years after dx
what is CTE?
abnormal tau protein buildup resulting from recurrent head injury
what are the 4 causes of secondary parkinsonism?
1) traumatic - chronic traumatic encephalopathy (CTE)
2) toxic
3) infectious
4) drug-induced -antipsychotics, digestive, or MPTP drugs
what are the effects of CTE?
memory, behavior, personality, speech and language, and balance disturbances
what is Huntington’s disease/Huntington’s chorea?
an autosomal dominant hereditary disorder that causes degeneration in many areas of the brain (predominantly in the striatum and cerebral cortex)
enlarged ventricles
dementia
when is the onset of Huntington’s disease?
30-40 y/o
after the onset of symptoms, how long do pts with Huntington’s disease have?
about 15 years
what happens to the PPN in Huntington’s disease?
it is disinhibited
t/f: Huntington’s disease is a dopamine problem
false
are D1 or D2 putamen receptors overactive in Huntington’s disease?
D1, causing upregulation of the go pathway and down regulation of the no-go pathway
what happens to D2 receptors in the putamen in Huntington’s disease?
they are degenerated leading to a down regulation of the no-go pathway
what happens to the GPi in Huntington’s disease?
it has reduced inhibition ???
what is the affect of the PPN being overly inhibitory in Huntington’s disease?
not enough activation of postural muscles
is clonus an UMN sign or LMN sign?
UMN sign
