Neuro Flashcards
(178 cards)
What are the UMN reflexes?
-Babinski
-Clonus
-Hoffman sign - middle finger - flick DIP of index or middle into flexion
Abnormal - reflex flexion of DIP of thumb and DIP of index or middle (whichever not flicked)
See hyperreflexia of DTR - used for UMNL
What are the disease specific measures for PD
PDQ-39 - parkinson’s disease questionnaire
UPDRS - unified PD rating scale
What are the motor strategies for postural control?
Ankle
Distal to proximal
Fixed support
Ankle joint is axis, fixed pendulum for shifting - small displacements
Forward - gastroc, hamstring, paraspinals
Back - tib ant, quads and abs
Hip
Proximal to distal
Fixed support
Head and hips move in opposite direction
Larger and faster which exceeds the limit of support
Use when task (not big enough for stepping) or environment (pool, balance beam)
In elderly
Forward sway - abs, quads
Backward sway - paraspinals, hamstring
Stepping
Re-establish new BoS to a new contact support surface
Change in support strategy
Large, fast displacements
Rapid steps or hops in direction of CoM
Lateral step - towards side falling
Crossover - other foot goes to step because of the weight shifting - easier to move but gets caught on feet and can cause falls especially in elderly
What is the seating system feature?
Tilt in space seating system
-shifts as one unit rearwards or upwards
-manual w/c - caregive, power w/c - user
-beneficial for individuals with fair to poor trunk control and unable to sit upright for long durations
-benefits - improves balance and head positioning, improves skin integrity and provides pressure relief, improve comfort
What are the interventions for abnormal tone, hypotonia and hypertonia?
Abnormal tone
-Stretching, casting, splinting, orthoses
-Sensory stimulation techniques
Hypotonia
-Decreased support
-Increased resistance
-Joint compression (axial - reflex for extensors) - not for down syndrome
-Manual facilitation techniques - tactile input
Hypertonia
-Increase support
-Modify tasks
-Positioning in lengthened position
-Heat (not for MS or sensory deficits)
What is poliomyelitis? Including characteristics and recovery
An acute infectious viral disease caused by poliovirus - enteric virus (of intestines) ingested through fecal-oral route. 5% attack motor cells in brainstem and spinal cord
Characteristics
LMN syndrome
Weakness/ paralysis may be patchy
Asymmetrical
LE>UE
Brainstem - less commonly affected
Partial or full recovery - up to 2 years
Leading to hypertrophy (of the other muscles, not the ones affected) and neuroplastic changes (sprouting of neighbouring terminal axons - reinnervate muscle fibres of muscle unit - take on bigger one)
What is the difference between idiopathic parkinson’s diease, parkinsonism and parkinson’s plus syndrome
idiopathic parkinson’s diease - chronic progressive neurogenerative disorder affecting dopamine production through the pars compacta of the substantia nigra in the basal ganglia (insidious onset, in 6th decade, etiology unknown)
basal ganglia is NOT an UMNL
Parkinsonism - a state of mimicking or appear to look like idiopathic PD without having PD
Parkinson’s plus syndrome - neurodegenerative disease that produce parkinsonism as well as other neuro S + S
What does a stroke examination consist of?
Cranial nerve integrity
Sensation - previous tests
Flexibility and joint integrity
-Contractures, ROM (wrist and shoulder specifically)
-Wrist edema - carpal bones malaligned = more prone to impingement in wrist
Motor function
Muscle strength
-ACA - affects LE, MCA - affects UE
-If you can’t isolate the muscle, MMT would be invalid
Postural control and Balance
-Balance impairments following a stroke - weakness, poor reactive/anticipatory, sensory loss, even weight distribution, delayed/abnormal contracture
-Fall towards hemiplegic side
-Assess static and dynamic in sitting and standing
-Use performance based or stroke specific tests (PASS, FIST)
Gait and locomotion
Integumentary integrity (Skin)
Aerobic capacity and endurance
Functional status
Stroke - specific intrsument
FMA
STREAM
Chedoke-McMaster
SIS
Describe impairments of motor planning of PD
Initiating movement
Freezing episodes - triggered by competing stimulus / stress
Hypomimia (masked face)
Poverty of movement - decrease in number and amplitude of movement
Micrographia - abnormally small handwriting
Describe posterior cerebral artery (PCA) syndrome. Including supply and characteristics
SUPPLIES
Occipital lobe, medial and inferior temporal lobe, upper brainstem (midbrain), posterior diencephalon (includes most of thalamus)
Posterior communicating artery - allows for perfusion of proximal PCA
Proximal to artery - minimal
Distal to artery - greater deficits
Common characteristics
Peripheral territory - amnesia, homonymous hemianopia, visual agnosia (difficult recognizing objects/ people), prosopagnosia (difficulty naming people), dyslexia, colour naming and discrimination
Central territory - central post-stroke (thalamic pain) - burning, intermittent shooting, severe, hemianesthesia, sensory impairments (all modalities), contralateral hemiplegia, oculomotor nerve palsy (helps control movement of eye)
How do you improve strength in someone with a stroke? Including precautions
Progressive strengthening resistance - no evidence of negative effects on spasticity and ROM
Combined with functional activities - assists with ADLs (GO WITH MOST FUNCTIONAL ONE ON PCE)
Precautions
Specially designed gloves or wrist weights - with poor hand function
Impairment sensation = increase injury risk
Postural deficit = increased falls risk
High incidence of hypertension and cardiac disease in patient with stroke (monitor S + S- might have caused it too)
What is the pathophysiology of a TBI?
Focal injury - non-penetrating (coup/contracoup) vs. penetrating
-Can have diffuse effects on focal injury
Diffuse axonal injury - widespread - shearing of axons - damage brain structures
Hypoxic - ischemic injury: due to constriction, disruption of blood vessels - also from systemic hypotension
Increased ICP
Please describe how the nervous systems works for sensory and motor function
See image in sensory and motor function section
What is GBS? Including pathophysiology and etiology
An autoimmune disease creating acute inflammation and demyelination of the cranial and peripheral nerves.
Due to autoimmune causes acute inflammation polyneuropathy creating problems with the Schwaan cells (produce myelin sheath) causing demyelination of the peripheral nerves. This leads to slowed, dispersed or blocked impulse conduction and if severe, axonal damage.
Etiology
-unknown
-Common after an infection or illness (common upper respiratory tract infection)
-Age 16-35 and 50-74
What is the pathophys of ALS?
progressive degeneration of motor neurons
-UMN in motor cortex and corticospinal tract
-Brainstem nuclei - CN V (trigeminal), CNVII (facial), CN IX (glossopharyngeal), X (vagus), XII (hypoglossal)
-LMN - anterior horn cells of SC
SPARED
-sensory system and spinocerebellar tracts
-brainstem nuclei of CNIII (occulomotor), CN IV (trochlear), CN VI (abducens)
-LMN - anterior horn cells for S2 (striated muscles of pelvic floor)
*can initially get axon sprouting but eventually progressive > redegeneration = function begins to rapidly decline
What are the two goals of neuro physio treatment?
Restorative function / impairments
Compensatory approach
*not mutually exclusive
What are gait abnormalities in those with PD?
Festinating gait - Cog foward to Los - have to take a step (due to stooped posture) - can be anteropulsive or retropulsive (backwards) - shortened stride with increasing speed
Freezing - suddent stop - worse with more attention demands
Shuffling steps- decrease hip flexion, knee flexion and ankle flexion
Decrease trunk rotation, arm rotation - rigidity
difficulty with dual task demands, increased attentional demands
How do you diagnose ALS?
-EMG, nerve conduction, muscle and nerve biopsies and neuroimaging
-Requires:
Presence of LMN by clinical exam, electrophysical or neuropathological or UMN by clinical exam - progression within a region or other region
Absence:
-other disease that may explain or neuroimagining that may explain
What are terms for sensory impairment?
Allodynia - non-noxious stimulus that produces pain
Analgesia - loss of pain sensitivity (inability to feel pain)
Causalgia - burning painful sensation, often along nerve distribution
Dysesthesia: touch sensation produces pain
Hyperalgesia: heightened sensitivity to pain
Hyperesthesia: heightened sensitivity to sensory stimulus
Hypoalgesia - decreased sensitivity to pain
Paresthesia: abnormal sensation with no apartment cause (numbness, tingling)
What is a UMN vs. LMN
UMN - originate in brain, SC, brainstem
Inform to LMN
Originate before anterior horn cell of SC
LMN - originate in cranial nerves nuclei and motor neurons
Originate after anterior horn cell of SC
Receives information and take toward muscle
Comparison - UMN vs. LMN
Weakness - Yes(Spastic), No (flaccid)
Atrophy - No, Yes
Fasciculations - No, Yes
Reflexes - Hyperreflexia, Hyporeflexia/Areflexia
Tone - Increased, decreased
What are the characteristics of ALS?
Depends on extent and location of ALS
UMN and LMN
Asymmetrical
Distal > proximal
Caudal > Cranial
What is the etiology of cerebellar lesions?
Damage to pathways and structures associated with the cerebellum
-Stroke - hemorrhagic (since it is messy) > ischemic
-TBI
-Hypoxic brain injury
-Nutritional disorder (vitamin B1 and/or vitamin B12) - B1 is thiamine
-Exogenous substance (alcohol - because it metabolizes B1, medication, industrial agents)
-Idiopathic disorders (olivopontocerebellar atrophy)
-Congenital disorder (arnold- chiari malformation -cerebellum descends into foramen magnum)
-Hereditary disorder (Friedreich’s ataxia - cerebellar and sensory ataxia)
-Hypothyroidism
-MS
What are the considerations required for prescriptive wheelchairs?
Patient-related factors
Environment-related factors
diagnosis-related factors
Function
Safety
How do you improve motor control and UE function in someone with a stroke
Focus on dissociation of segments and selective out-of-synergy movements
As close to normal as possible
Help to guide movement and use facilitation techniques - active control ASAP
Task-orientated practice - using affected limb
-Modified plantagrade - weight bearing through arms over table - LE does movement
Constraint induced movement therapy (CIMT) - increased use of affected UE (other is tied)