Exam 1 Info Flashcards
stroke
sudden loss of neurological function caused by a lack of blood flow to the brain
-signs/symptoms > 24 hours
transient ischemic attack
temporary impairment of blood flow
-signs/symptoms < 24 hours [usually minutes to hours]
causes of an ischemic stroke
- thrombus (blood clot)
- embolus (blood, plaque, or other matter)
- hypotension
Which artery is normally involved with the ischemic stroke?
MCA
lacunar stroke
- small vessels involved, can be purely motor or purely sensory
- tends to have better outcome (b/c small artery)
- deep in the white matter of the brain
hemorrhagic stroke
- blood vessel rupture leading to decreased blood to downstream structures & pressure on nearby structures
- can be intra-cerebral or subarachnoic
potential causes for hemorrhagic stroke
- aneurysm
- arterial-venous malformation
aneurysm
-dilation in a blood vessel
list of general risk factors for stroke
- exercise
- diet
- blood pressure
- cholesterol
- diabetes
- smoking
- atrial fibrillation
- family history
arteriovenous malformation
abnormal collection of small arteries
time frame of being able to use t-PA
if stroke occurred less than 3 hours previously
signs/symptoms of stroke
- focal weakness
- speech impairments
intracerebral hemorrhage signs/symptoms
progressive worsening of signs and symptoms with loss of consciousness
angiogram
- invasive test (requires insertion of catheter & dye)
- used to image blood vessels
- not good for acute strokes due to the time it takes to administer
CT
- computed tomography
- generally good for imaging mass lesions
- best choice for detecting subarachnoid hemorrhage
- not as sensitive for detecting ischemic strokes
MRI
- magnetic resonance imaging
- T2 best for detecting pathologies (more water present)
Which imaging is preferred for detecting ischemic strokes?
MRI
diffusion weighted MRI
- can detect ischemia within minutes of inclusion
- highly sensitive & specific in diagnosing ischemic stroke
multi-infarct dementia
- multiple small strokes deep in white matter
- associated with advancing age and HTN
- cause dementia
- chronic
- neuronal tissue decreasing
- motor function is fine but generally more confused state of mind
thrombolysis
- is the breakdown (lysis) of blood clots by pharmacological means, and commonly called clot busting
- t-PA
- indicated for patients with an ischemic stroke within 3 hours of onset
- does not affect mortality but does help with reduction of disability/mobility months later
ischemic stroke cascade
circulatory arrest -> focal infarction -> release of neurotransmitters -> altered metabolism with depolarization -> brain cells cease to produce energy -> influx of calcium -> free radical formation -> release of nitric oxide & cytokines -> further damage to brain cells
ACA syndrome
- contralateral hemiparesis & sensory loss
- LE more involved (due to homunculus)
- personality & behavioral changes
MCA syndrome
- contralateral hemiparesis & sensory loss
- UE more involved
- speech/language impairments OR perceptual problems [determined by which side of the brain is dominant]
internal carotid artery syndrome
- produces massive infarct of MCA & can impact ACA
- significant edema is common & can result in herniation, coma & death
- massive infarct & with an entire hemisphere affected there is not big opportunity for neuroplasticity [which is why the edema can easily come in]
PCA syndrome
- signs/sx depend on location of occlusion
- if proximal to PCA = minimal deficits
- if distal to PCA = sensory loss, thalamic pain, homonymous hemianopsia, certain agnosias, cortical blindness, memory loss
- big sign/sx is pain & visual problems
vertebrobasilar artery syndrome
- vertebral arteries: cerebellum & medulla
- basilar artery: pons & cerebellum
- highly complex b/c of arteries coming off of basilar, etc.
locked-in syndrome
- complete paralysis w/ some preservation of eye movement
- full blown stroke of the basilar artery
positive symptoms
- “release” of abnormal behaviors
- brainstem does not receive inhibition messages & therefore does whatever it wants
What do positive symptoms lead to?
- presence of abnormal reflexes
- increased DTRs
- spasticity
negative symptoms
-a loss of normal behaviors
What do negative symptoms lead to?
-weakness (plegia vs. paresis; hemi, tetra, para, incomplete or complete etc.)
primary impairments
- those due directly to the CNS insult
- largely dependent on lesion location so highly variable
list of motor system impairments
-weakness, abnormal synergies, abnormalities of tone, co-activation, poor coordination, hypokinetic & hyperkinetic disorders
list of non-motor impairments
-sensation (including vestibular function), perception, vision, cognition & behavior
motor control impairments & CNS involvement with cerebral cortex
- hemiplegia
- tonal abnormalities
- loss of selective movement
motor control impairments & CNS involvement with basal ganglia
- movement disorders
- rigidity
- athetosis
- chorea
- dystonia
- hemiballismus
athetosis
a condition in which abnormal muscle contractions cause involuntary writhing movements. It affects some people with cerebral palsy, impairing speech and use of the hands
hemiballismus
violent writhing and muscle spasms involving one side of the body, usually caused by a lesion of the subthalamic nucleus of the opposite side of the brain
motor control impairments & CNS involvement with cerebellum
-ataxia
hemiplegia
- weakness on one side of the body
- pts with UMN lesions
- loss of input from descending tracts
strength
- ability to generate sufficient tension in a muscle
- number & type of motor units recruited & firing frequency
weakness
- inability to generate sufficient levels of force
- due to loss of input from descending motor pathways -> decreases excitatory drive to motor units -> decreased ability to recruit & modulate motor neurons
muscle tone
-characterized by a muscle’s resistance to passive stretch
How is muscle tone assessed?
-through PROM, observation (posturing), & DTRs
flaccidity
- abnormality of muscle tone
- limb feels heavy & limp
- weak
- present immediately post stroke due to cerebral shock & can last days to weeks (could persist esp in pts with cerebellar lesions)
visual/perceptual sensory abnormalities
- neglect
- homonymous hemianopsia
spasticity
velocity dependent increase in muscle tone/tonic stretch reflexes
synergistic movement
problem in activating & sequencing appropriate muscles = production of unwanted stereotypical movements
-reflects the lack of fractionation & loss of selective movement
list of 7 ways to characterize spasticity
- hyperactive DTRs
- abnormal posturing
- excessive coactivation
- associated movements
- clonus
- stereotypical/synergistic movement
- clasp-knife response
UE flexor synergy pattern
- scapular elevation/retraction
- shoulder abd & ER
- elbow flex
- forearm supination
- wrist & finger flex
UE extensor synergy pattern
- scapular protraction
- shoulder add & IR
- elbow ext
- forearm pronation
- wrist & finger flexion
LE flexor synergy pattern
- hip flex, abd, ER
- knee flex
- ankle DF & inv.
- toe ext.
LE extensor synergy pattern
- hip ext, add, IR
- knee ext
- ankle PF & inv.
- toe flex
Brunnstrom’s Stages of Recovery
- flaccid paralysis
- minimal movement in synergy
- voluntary movement - synergistic
- some movement out of synergy
- movement almost independent of synergy
- normal movement
impairments of secondary progressive MS
- weakness
- mild hypotonia
- fatigue
- poor coordination
- ataxia
- intention tremor
- short term memory loss
dysmetria
-errors in range & direction of movement
decomposition
-altered movement trajectories with tendency to move one joint at a time
dysdiadochokinesia
-inability to sustain rhythmic movements
impairments of Parkinson’s Disease
- hypokinesia = bradykinesia, resting tremor, rigidity
- postural abnormalities
- oral motor impairments
- slightly slowed cognitive thinking
bradykinesia
- slowed movement time
- decreased amplitude
two types of rigidity (hypertonicity)
- lead pipe
2. cog wheel
athetosis
- slow, involuntary, writhing or twisting movements
- accompanies cerebral palsy
- can have fluctuations in tone & movement patterns
- may occur with spasticity, chorea, or tonic spasms
- any body part but mostly seen in UEs
chorea
involuntary, rapid, irregular, jerky movements
dystonia
-sustained muscle contraction; twisting & repetitive
ballismus
-large violent proximal limb movements
3 levels of task oriented approach to the examination
- functional: ability to perform given tasks [interview-based, performance-based]
- strategy [movement patterns used, organization of sensory & perceptual information]
- impairment [motor, sensory, cognitive, perceptual; multi-system impairments such as gait, balance, posture]
MDC
- smallest amount of change that can be considered above the threshold for error in the measurement
- minimal detectable change
MCID
- smallest change in an OM that is perceived as beneficial by the patient & that would not lead to a change in the patient’s medical management
- minimal clinically important difference
responsiveness
-ability of a test to measure change (minimal detectable change and minimally important difference or minimal clinically important difference)
multiple sclerosis defined
-chronic inflammatory, demyelinating disease of the central nervous system
Charcot’s triad
-paralysis & cardinal symptoms of MS including intention tremor, scanning speech, and nystagmus
onset of MS
-typically occurs between ages of 15-50 years with peak at age 30
Is MS more common in men or women?
-women by a 2:1 ratio
Which ethnicity has highest reported rates of MS developing?
-white populations
etiology of MS
-precise etiology is unknown BUT thought to be an autoimmune disease induced by a viral or other infectious agent
pathophysiology of MS
-normal immune response to a virus up to a point where the T-lymphocytes (that are myelin-sensitive) go through the blood-brain barrier & attack the myelin
myelin
- insulator that speeds up the conduction along nerve fibers from one node of Ranvier to another
- also serves to conserve energy for the nerve b/c depolarization occurs only at the nodes
mass effect
- abnormally high pressures
- in MS this is caused by local inflammation, edema, & infiltrates that surround the acute lesion
oligodendrocytes
-myelin-producing cells
Which type of MS (of the 4 types discussed in class) appears to be associated exclusively with disease of the oligodendrocytes?
-primary-progressive MS
gliosis
-proliferation of neurological tissue within the CNS & results in plaques or glial scars
retrograde degeneration
-stage of degeneration where the axon itself becomes interrupted & begins to die
primary place in CNS that is affected by MS
-primarily white matter
list of areas of involvement in CNS with MS
- white matter
- optic nerves
- periventricular areas
- cerebellar peduncles
- spinal cord [corticospinal tracts & posterior columns]
relapsing-remitting MS (RRMS)
- most common course affecting approximately 70% of patients with MS
- characterized by clearly defined disease relapses (periods of acute worsening of neurological function) followed by remissions (periods w/o disease progression & partial or complete abatement of signs/symptoms)
secondary progressive MS (SPMS)
-begins with a relapsing-remitting course followed by progression with or without occasional relapses, minor remissions, & plateaus
progressive-relapsing MS (PRMS)
- begins with progressive disease course from onset, with clear, acute relapses that may or may not resolve with full recovery
- intervals between relapses are marked by continuing disease progression
primary progressive MS (PPMS)
- rare form occurring in about 10% of cases
- characterized by a nearly continuous worsening of the disease from onset without distinct relapses
- typically later onset, usually after age 40
benign MS
-characterized by mild disease in which patients remain fully functional in all neurological systems 15 years after disease onset
malignant MS (Marburg’s variant)
-characterized by rapid progression leading to significant disability of death within a relatively short time after onset
exacerbations (MS relapses)
-defined by new & recurring MS symptoms that last at least 24 hours & are unrelated to another etiology
pseudoexacerbation
- refers to temporary worsening of MS symptoms
- typically comes & goes quickly, usually within 24 hours
Uthoff’s symptom
- adverse reaction to heat that a majority of individuals with MS demonstrate
- anything that raises the body temperature can bring on an attack
clinically isolated syndrome (CIS)
-first clinical episode indicating possible demyelinating disease
characteristics of CIS
- involves young individuals (25-40 yrs)
- acute to sub-acute onset with peak reached within 2-3 weeks
- isolated in time
- typically monofocal signs indicating lesion in optic nerve, SC, brainstem, or cerebellum
- 50-70% have multiple brain lesions on MRI
MS related impairments (most common to least common)
- poor balance & mobility
- LE weakness
- fatigue
- poor bladder control
- poor concentration or forgetfulness
- bowel irregularity
- pain
- depression
- visual impairment
What is the most common problem reported in MS?
-fatigue (overwhelming sense of tiredness, lack of energy, feelings of exhaustion)
peripheral fatigue in MS
- muscle fatigue
- Secondary to exertion
- not present at rest
- late in disease course
central fatigue in MS
- progressive decline in ability to drive muscles maximally
- affects arousal & attention
- feeling of constant exhaustion
- not related to changes in sensory & motor pathways
pathophysiology of fatigue
- BG or widespread axonal damage
- impairment of volitional drive to motor pathways
- over-activation of frontal cortical areas during movement preparation [supplementary motor area, dysfunction between thalamic-BG-frontal cortex circuits, increases perception of effort even with submax exercise]
weakness & MS
- common impairment with MS
- more severe in LEs
- affects both generation force & muscle endurance
- related to corticospinal tract abnormalities
- patients with UMN lesions: weakness more a problem than spasticity
spasticity & MS
- due to combination of neural & muscular changes
- causes velocity dependent increase in resistance to stretch
- secondary impairment: decreased ROM due to reduced muscle fiber length & decreased number & length of sarcomeres
- changes in fiber type also occur: may affect muscle recruitment
ataxia & MS
-incoordination of movement due to sensory or cerebellar involvement
patients with cerebellar lesions
- difficulty with predicting movement
- problems with adapting movement to new circumstances
prognosis of MS
- life expectancy typically unchanged
- yet, functional decline is expected over time
- 10 years: majority of pts able to work
- 15 years: 50% need assistive device to walk
- 20 years: 50% require wheelchair
positive prognostic indicators influencing short-term prognosis for MS
- mild to moderate impairment
- intact cognition: increases probability of improving on RMI
- intact sphincter control
negative prognostic indicators influencing short-term prognosis for MS
- more severe disease - 10% improvement
- cognitive impairment
- disease duration
factors influencing long-term prognosis for MS
- male gender
- older age (> 40) at onset
- motor, cerebellar, sphincter problems at disease onset
- multifocal disease at onset
- frequent attacks within first 5 years
- short interval between first 2 attacks
- shorter time to reach EDSS = 4
- progressive course
requirements to confirm MS
- dissemination in space: 2 lesions in CNS
- dissemination in time: evidence showing lesions occurred at different times, > or equal to one month apart
- rule out other diagnoses
interferons as medication for MS
- slow immune system by reducing inflammation, swelling & T & B cell proliferation -> reduce frequency & severity of exacerbations
- block T cells from crossing blood-brain barrier
Which type of MS would benefit most from using interferons for medication?
-relapsing-remitting to reduce the number & frequency of exacerbations
Parkinson’s Disease Defined
chronic, progressive CNS disorder
Cardinal Signs of PD
Bradykinesia
Rigidity
Tremor
Postural Instability
Parkinson’s Population
Affects >/=2% of population >65yo
Average onset=40-60
Parkinsonism
group of disorders related to abnormal basal ganglia function
3 Classifications of Parkinsonism
- Ideopathic PD (most common)
- Parkinson’s due to known causes (tumor, infection, virus, toxins, drugs)
- Parkinson’s Plus Syndromes
Striatum Made up of:
Caudate
Putamen
Basal Ganglia Inhibits the:
Brainstem (reticular formation)
Basal ganglia excites the:
Motor cortex
Basal ganglia loops
- Direct
- Indirect
Direct Loop
Excitatory–increases movement
Indirect Loop
Inhibitory–decreases movement
Basal Ganglia Function
initiation and modulation of movement
Substantia Nigra
Part of BG that produces dopamine for movement
Damage to substantia nigra–>
Increased inhibition to cortex–>bradykinesia
Decreased inhibition to brainstem–>increased postural tone=rigidity
PD Clinical Presentation
- Insidious onset
- Gradual progression
- 2 subgroups (postural instability/gait dysfunction and Tremor predominant)
Rigidity
- Hypertonia (increased resistance to stretch) due to co-contractions on agonist/antagonist
- usually bilateral (asymmetrical early on)
- non-velocity dependent
- proximal>distal (lots in trunk)
- 2 Types (cog wheel/lead pipe)
Bradykinesia
- Reduced movement (speed, amplitude, range)
- Hypokinesia–>akinesia
- Freezing
Freezing
- Sudden break or block of movement
- giving pt targets or visual cues work well
resting tremor
- Rhythmic oscillations (4-6Hz)
- Diminishes with movement of that body part
- Increases with stress, anxiety, fatigue
Postural Instability
- One of most common Sx of PD
- Decreases QOL
Factors Contributing to Postural Instability
- Rigidity
- Poor anticipatory control
- inflexible motor responses to pertrubations
- decreased muscle torque and speed of contraction
- problems with dual-tasking
- visuospatial impairment
PD Cognition/Perception impairments
- mild to severe
- slowed processing/thining
- loss executive function
- impaired vertical perception
- impaired topographical orientation
- impaired body scheme and spatial relations
PD Behavior impairments
- Hallucinations
- Delusions
- Mood disorders
- Anxiety
- Social withdrawal
- depression
Other PD Impairments
- Paresthesias
- pain
- speech/swallowing
- ANS dysfunctin (thermoreg, seborrhea, slowed pupillary response, bowel/bladder, sexual dysfunction)
- Cardiopulm (orthostatic hypotension, pneumonia)
Motor Planning Problems
- Prolonged movement start times
- Freezing
- difficulty performing complex, sequential movements
- poor control with learned motor skills
- freezing
Motor Learning problems
- Procedural learning (especially complex)
- random practice
- Dual tasking
PD type with worse prognosis
Postural instability/gait disorder
Hoehn & Yahr
Track PD progression
PD Diagnosis
- based on history and clinical S/Sx
- 2 of 4 cardinal signs
- no diagnostic test
Goals of PD management
- Slow disease progression (neuroprotective agents)
- Symptom management
- Prevention of compications
PD drug classifications
- Neuro-protective
- Anticholinergic
- Dopamine Replacement
- Dopamine Agonist
Sinemet
- PD drug
- Dopamine Replacement
- Decrease bradykinesia and rigidity
- Side effects
- Loss of effectiveness after 5-7years
- on/off phenomena
Surgical Management of PD
- Thalamotomy/Pallidotomy
- deep brain stimulation
Diagnostic Tests for MS
- MRI
- CSF Analysis (increased immunoglobulin)
- Evoked Potentials (slow NCV)
Best Test for Ischemic Stroke
-Diffusion Weighted MRI
Best Test for Hemorrhagic Stroke
-CT
Best Test for TBI
-MRI better resolution than CT
