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Upper Motor Neuron (UMN) vs. LMN Tone
UMN lesions cause increased velocity-dependent spasticity; LMN lesions cause decreased tone (hypotonia).
Basal Ganglia vs. Cerebellar Muscle Tone
Basal ganglia lesions produce non-velocity-dependent rigidity; cerebellar lesions present with normal or decreased tone.
diagnoses of UMN
stroke, sci, tbi, cerebral palsy, MS, ALS
diagnoses of LMN
GBS, PNI, radiculp, polio, ALS
diagnoses of basal ganglia
parkinson
diagnoses of cerebellum
stroke, tumor
Parkinson's Disease (PD) Pathology
Progressive neurological disorder caused by dopamine depletion in the substantia nigra.
Parkinson's Disease Cardinal Signs (TRAP)
Tremor (resting), Rigidity (cogwheel/lead-pipe), Akinesia/Bradykinesia, and Postural instability.
what are some other S/S of parkinsons
Early symptoms:
⢠Loss of smell
⢠Constipation
⢠Sleep disorders
Motor: Hypophonia, mask-like face, micrographia
Cardio: Orthostatic hypotension, fatigue, weakness
Respiratory: Restrictive lung disease due to decreased chest expansion
Cognition/Behavior: Difficulty with dual tasking, depression, dementia
what does cogwheel vs lead pipe ridigity
lead pipe: smooth consistent
cogwheel: jerky, ratchet
Gait Characteristics in Parkinson's Disease
Festinating/shuffling gait (postural), decreased step length/width, reduced trunk rotation, and freezing of gait (sudden inability to move).happens from cognitive overload, and en bloc turning (robot like, body moves together)
strategy to help for freezing of gait
what about festinating gait?
distraction. like drop a tissue or look at the door
give them a heel under toes like a wedge to put more wgt on heels to help with posture and lean back more
Hoehn and Yahr classification of disability
I Minimal or absent; unilateral if present.
II Minimal bilateral or midline involvement.
Balance not impaired.
III Impaired righting reflexes. BALANCE IMPAIRED
Unsteadiness when turning or rising from chair.
Some activities are restricted, but patient can live independently and continue some forms of employment.
IV All symptoms present and severe. Standing and walking possible only with assistance.
V Confined to bed or wheelchair.
intervention for parkinson
Caregiver education
⢠Gait training
̶ Metronomes, music, visual cues, one step
commands when freezing/frozen
⢠Posture:
̶ Rotation exercises and crossing midline
̶ Prone lying
⢠Hypokinesia:
̶ BIG movements
̶ Stretching/ROM/chest mobility
⢠Balance training
⢠Tai chi, yoga, cycling, dance therapy
What are the key facts about Levodopa/Carbidopa in Parkinson disease?
ā Gold standard medication for Parkinson disease
Levodopa crosses the blood-brain barrier and is converted to dopamine.
Carbidopa prevents levodopa breakdown in the periphery, allowing more levodopa to reach the brain and reducing side effects.
š§ Memory Trick: "Carbidopa = Car Pool." š
Carbidopa escorts (car-pools) levodopa safely to the brain
What is the "on/off phenomenon" with Levodopa/Carbidopa?
On Phase:
Medication is working
Dyskinesia (excessive involuntary movements) may occur
Off Phase:
Medication wears off
Dystonia (muscle stiffness/cramping) and worsening Parkinson symptoms occur
š§ Memory Trick: "ON = Overmoving; OFF = Frozen."
ON ā Dyskinesia = too much movement
OFF ā Dystonia = stiff/frozen
What are the PT considerations for a patient taking Levodopa/Carbidopa?
š Schedule PT about 1 hour after the medication dose (during the "on" phase).
š„© A high-protein diet decreases levodopa effectiveness because amino acids compete for absorption and transport into the brain.
š§ Memory Trick: "1 Hour = Power š¶"
Treat when the medication is working best.
"Protein Prevents Parkinson Pills." š„©āš
Dyskinesia vs dystonia
Involuntary, repetitive, smooth,
muscle movements
⢠e.g., snake-like twisting of arm
⢠Affects large muscle groups
(arms, head, trunk, legs)
⢠Not usually painful
⢠ON phase
DYSTONIA
⢠Prolonged, involuntary muscle
contractions; muscle spasm
⢠e.g., toe curling
⢠Affects a specific muscle or group
of muscles
⢠Causes pain
(sometimes debilitating)
⢠OFF phase
Multiple Sclerosis (MS) Pathology
Autoimmune disease marked by progressive demyelination of central nervous system (CNS) neurons.
UMN LESION
s/s of MS
Motor: Spasticity (UMN lesion)
⢠Sensory: Numbness and paresthesia
⢠Gait: Scissoring, extensor spasticity in LE, ataxia, uneven steps
⢠Bladder: Spastic, flaccid
⢠Speech and Swallowing: Dysphagia (difficulty swallowing), dysphonia (difficulty
with voice production)
⢠Cognition: Diminished attention, concentration
⢠FATIGUE
⢠Optic Neuritis, Trigeminal Neuralgia
⢠Cerebellum: Nystagmus, coordination, balance, ataxia, intention tremor
⢠Emotion: Pseudobulbar affect (inappropriate laughing or crying)
what are unique s/s of MS to distinguish between which UMN lesion it is?
LUCC
1. Lhermitte's Sign (neck flexion cuz electric sensation down spine)
to remember think MESSY HAIR. when you flip your neck forward (so neck flexion) your hair will be messy
2. Uhthoff's Phenomenon (heat intolerance) temporay (24 hrs) pseudo exacerbation
to rememeber think "U turn Heat OFF"
3. Charcot's Triad (scanning speech, intention tremor, and nystagmus) SIN
4. Cranial Nerve- II (inflammation of optic nerve so optic neuritis and pupillary light reflex so in MS with light pupils will dilate (marcus gunn pupil)
diff type of MS
⢠Relapse-Remitting RR: Short duration
attacks with full or partial recovery, may or
may not leave lasting symptoms/deficits
̶Most common form (about 80%)
⢠Primary Progressive: Steady increase in
disability without attacks/exacerbations
⢠Secondary Progressive: Initially RR, then
symptoms increase without periods of
remission
⢠Progressive Relapsing: Steady increase in
disability with superimposed attacks
what was changed in 2013 for MS types
they dont use the term progressive relapsing anymore instead is called clinically isolated syndrome (⢠First episode of inflammatory demyelination in the CNS
⢠Could become MS if additional activity occurs
⢠TWO types:
1. Not active - No additional MRI activity
2. Active - With additional MRI activity >>> Relapse- remitting)
Physical Therapy Exercise Guidelines for MS
Exercise 3-5 days/week at low intensity in cool environments; schedule sessions in the morning to avoid fatigue. for 30 min and can do cycle, walk, swim
Amyotrophic Lateral Sclerosis (ALS) Key Feature
Degeneration of both upper and lower motor neurons without sensory involvement.
A-ALS LEAVES SENSATION
common s/s of ALS
UMN & LMN presentation without sensory loss
̶Muscle atrophy, fasciculations (LMN)
̶Spasticity, hyperreflexia (UMN)
̶Dysphagia, dysarthria (Bulbar)
⢠ONLY motor neurons will be affected
⢠Cognition: Dementia, attention deficits
⢠Emotion: Pseudobulbar affect- emotional lability
⢠Muscles: Cervical spine extensors weakness is
common
⢠Respiratory muscle weakness ----> DEATH!
diff between ALS vs MS
ALS- motor only, yes likes neck flexion, 9/10/12 CN
MS- affects sensory, CN2 and no neck flexion!
ALS interventions
Medical Management
⢠No effective treatment for disease
PT Management
⢠Focus on functional activities/ADLs and energy conservation initially and end
stages
⢠Recommend soft foam collar for neck if weakness is present
⢠Maintain respiratory function, breathing exercises
⢠Avoid over fatiguing
̶Take frequent breaks during activities, energy conservation techniques
⢠ROM, positioning if needed
Guillain-BarrƩ Syndrome (GBS) Pathology
Acute autoimmune inflammatory demyelinating polyradiculoneuropathy affecting peripheral and cranial nerves post-infection.
LMN LESION- periphral nerve is affected
S/s of GBS
Motor loss/paralysis:
̶DISTAL TO PROXIMAL
̶Rapid and progressive
⢠Sensory loss:
̶Glove and stocking
̶Burning, tingling, numbness
⢠Decreased reflexes/Areflexia
⢠Respiratory and cranial involvement:
VII, IX, X, XI, XII
⢠Fatigue
GBS-glove stocking appearance and bilateral
Guillain-BarrƩ Syndrome Clinical Progression
Symmetrical, rapid motor weakness progressing in a distal-to-proximal ascending pattern with areflexia.
Initial Interventions for Guillain-BarrƩ Syndrome
Maintain respiratory care, prevent joint contractures, and use low-to-moderate intensity exercises to prevent overuse.
6-12 mths can recover