Exam VIII Flashcards
Common etiologies of CVA
thrombus (gradual onset), embolism (sudden onset), hemorrhage, TIA
Where to atherosclerotic plaques tend to form?
tend to form in vessels with angulations, constrictions, dilations or bifurcations
Factors controlling blood vessel diameter
increased [CO2] & [H+], decreased [O2] = vasodilation
vasoconstriction = opposite
Factors controlling blood vessel diameter
increased [CO2] & [H+], decreased [O2] = vasodilation
vasoconstriction = opposite
Factors controlling blood vessel diameter
increased [CO2] & [H+], decreased [O2] = vasodilation
vasoconstriction = opposite
CVA Signs/Sx
Flaccidity, Motor and Sensory Loss (hemiplegia and paresis), Spasticity, deveopment of obligatory synergies, hyperreflexia and return of primitive cutaneous and tonic reflexes, associated reactions, impaired righting/equilibrium/protective extension reactions, homonymous hemianopsia, cognitive/perceptual problems, speech and swallowing difficulties
Flaccidity
Thought to be due to abrupt disconnection of UMN’s & LMN’s (diaschisis), can last days, weeks or months
Motor/Sensory loss predominately of LE
CL paracentral lobule; CL anterior cerebral artery.
Motor/Sensory loss predominately of UE
CL pre and post central gyri; CL middle cerebral artery
Paresis
Related to the location and size of the brain injury. Mild weakness often on unaffected side due to fibers of LCST that remain IL
What is spasticity thought to be due to
disinhibition of the reticulospinal tract causing excessive muscle contractions of muscles involved in synergistic patterns that are normally inhibited.
UE Spasticity Pattern
Scapular retraction, shoulder adduction/IR, elbow flexion, forearm pronation, wrist/fingers flexion
LE Spasticity Pattern
hip adduction/extension/IR, knee extension, ankle PF
What is posture of right UE (d/t spasticity) due to
contracture, weak actin-myosin bonds, disinhibition of reticulospinal trect
Extension of right LE (d/t spasticity) due to
Unopposed input to LE LMN’s by reticulospinal & vestibulospinal tracts (these are not totally dependent on cortical control)
Extension of right LE (d/t spasticity) due to
Unopposed input to LE LMN’s by reticulospinal & vestibulospinal tracts (these are not totally dependent on cortical control)
What is an obligatory synergy?
Mass patterns of movement elicited by attempts at voluntary movement, reflexes, coughing/sneezing
Synergy Patterns
Could be d/t decreased corticospinal input on LMN’s & unopposed vestibulospinal, rubrospinal & reticulospinal input on LMN’s
Reticulospinal tract
originates in reticular formation of brainstem, projects bilaterally down through the ventral funiculus to postural muscles & gross limb muscles
What are abnormal reflexes though to be due to?
release of normal inhibition by UMN’s.
What do abnormal reflexes interfere with?
attempts of volitional movement and with functional mobility. (hyperreflexia, return of cutaneous reflexes, return of tonic reflexes)
Homonymous Hemianopsia
loss of half of visual field. Left = loss of left visual field.
Contraversive pushing
pt pushes toward the paretic side, often involves lesion in thalamus and/or roght sided cortical lesions causing neglect, can resolve in 6 mo.
Perseveration
continuous repetition of words, lesions in the premotor and prefrontal cortex.
Left CVA (right hemiparesis) Behavioral differences
difficulties in communication and processing information in a sequential manner, cautious/anxious/disorganized, hesitant to try new tasks, realistic regarding their dysfunctions
Right CVA (left hemiparesis) Behavioral differences
difficulty grasping the whole idea of a task, quick and impulsive, overestimate their abilities, safety more of a concern
Early warning signs of stroke
- Sudden N/T in face and/or extremities
- Sudden confusion and trouble speaking
- Sudden difficulty seeing out of one eye
- Sudden dizziness and LOB
- Sudden severe headache
Ischemic umbra
core area of irreversible neuronal damage.
Ischemic penumbra
peripheral area of “damaged” neurons (neurons that are vulnerable to extend the stroke) generally takes place in 1st 3-4 hours
Lacunar strokes
can affect neuronal cell bodies in the cerebrum, can affect internal capsule (capsular stroke)
Pure motor Sxs affects the
posterior limb of internal capsule, basalar pons or pyramids
Pure Sensory Sxs
affects the thalamus or thalamocortical fibers
Stage 1 of recovery from CVA
Initial flaccidity; no voluntary movement
Stage 2 of recovery from CVA
Emergence of spasticity, hyperreflexia and synergies
Stage 3 of recovery from CVA
Strong spasticity; voluntary movement possible, but only in synergistic patterns
Stage 4 of recovery from CVA
Decline in spasticity and synergies; voluntary control in isolated joint movements emerging
Stage 5 of recovery from CVA
Increased voluntary control out-of-synergies; coordination deficits present
Stage 6 of recovery from CVA
Control and coordination near normal
Stage 6 of recovery from CVA
Control and coordination near normal
Multiple Sclerosis
De-myelination of axons in CNS b/t ages 15-50
What is MS due to?
immune reaction triggered by a viral infection (possibly Epstein-Berr), Vitamin D deficiency could be a factor. Women 3x more effected
Sensory impairments in MS
parasthesias (face, trunk, extremities), decreased position sense, decreased pallesthesia, dysesthesias (burning/aching), Allodynia (light touch causes pain), trigeminal neuralgia, pain, lhermitte’s sign
Lhermitte’s Sign
- “electric-shock” like pain down the spine during flexion of the neck
- Possibly caused by “cross-talk” between de-myelinated axons in the white matter of the spinal cord; flexion of neck moves the cord up and causes rubbing of these axons
Optic Neuritis
inflammation/demyelination of the optic nerve, often first signs of MS.
Optic Neuritis Symptoms
- Pain posterior to eye with movement
- Blurred vision
- Scotomas (blind spots)
- Difficulty seeing in bright light
- Difficulty seeing objects of low contrast
Motor Impairments of MS
Fatigue, UMN S/S, Paresis, Ataxia, Dysmetria, dysdiadochokinesia (intention tremors), dysphagia, dysarthria, dysphonia
Cognitive/Behavioral Impairments of MS
More related to location of lesions vs severity of disease
Depression
Memory
Attention & learning
Conceptual reasoning
Poor executive functions (planning, organizing, problem solving)
Labile
Anxiety
Bowel/Bladder dysfunction
Sexual dysfunction (impotence, decreased libido)
Cognitive/Behavioral Impairments of MS
More related to location of lesions vs severity of disease
Depression
Memory
Attention & learning
Conceptual reasoning
Poor executive functions (planning, organizing, problem solving)
Labile
Anxiety
Bowel/Bladder dysfunction
Sexual dysfunction (impotence, decreased libido)
Relapsing/remitting
Onset of Sx w/ either full or partial recovery followed by periods of no progression of the disease (when deficit aways resolve b/t episodes = benign)
Secondary Progressive
initial relapsing/remitting course followed by progressive course (50% by 10 years, 90% by 25 years)
Primary Progressive
progresses consistently from initial onset, may have occasional plateaus & minor improvements
Progressive Relapsing
Progressive decline with episodes of increased symptoms. Least common
Clinically isolated syndrome
Person has an attack suggestive of demyelination but does not fulfill the criteria for MS
30%-70% will later develop MS
Should be started on immune-modulating drugs immediately
Signs/sxs of MS can be exacerbated by
- Heat = Uhthoff’s Phenomenon (increased body temperature worsens sxs) possibly due to affect on membrane channel proteins)
- Stress
- Viral or bacterial infections
Diagnosis of MS
evidence of plaques in 2 different areas, which occurred at different points in time.
two or more attacks of MS S/S during 2 time patterns (2 lasting @ least 24 hours, chronically progressive episodes @ least 6 mo)
ALS
Degeneration and loss of motor neurons in the spinal cord, brainstem and cortex
- results in UMN & LMN signs/Sx
ALS Signs/Sx
Both UMN & LMN
LMN: weakness/atrophy, fasciculations (contraction of motor units) respiratory impairments (dyspnea)
UMN: spasticity, hyperreflexia, dysarthria, dysphagia, cognitive impairments (frontotemporal dementia), sialorrhea (drooling)
Limb onset ALS
limbs affected first
Bulbar onset ALS
dysarthria & dysphagia affected first
Stages of ALS
I) mild focal asymmetric weakness; hand cramping
II) moderate weakness in groups of muscles
III) severe weakness, but ambulatory
IV) severe weakness; predominately uses w/c
V) severe weakness with loss of head control; spasticity noted
VI) bedridden with progressive respiratory distress
TBI
- Injury to the brain from an external force
- The leading cause of death and disability in young adults (1.5-2 million/yr).
50% MVA; 25% falls; 15% assaults/violence; 10% sports (Typical age 15-24)
Focal injury TBI
Local injury to brain tissue directly under the impact (coup injury) and/or at a site opposite the injury (coup-contrecoup injury)
Diffuse axonal injury (DAI)
Shearing, tearing and retraction of axons (white matter such as the internal capsule)
Mechanisms: acceleration/deceleration or rotational forces
May result in coma
What is normal ICP?
4-15 mmHg.
Possible NM impairments from TBI
- Abnormal tone
- Primitive postures (decorticate or decerebrate rigidity)
- Altered proprioceptive, vestibular and/or visual sensation (poor balance)
- Abnormal motor control (hemiparesis, decreased coordination, synergistic patterns)
Dysphagia (impaired swallowing)
Aphasias (expressive, receptive, global)
Possible Cognitive impairments from TBI
Altered level of consciousness Memory deficits Perceptual deficits (ideational/ideomotor apraxias, spatial neglect)
Possible Behavioral impairments from TBI
- Uncontrolled aggression, depression, frustration, anger
- Sexual and emotional disinhibition
Subcortical White matter
associational, projection, commissural fibers
Associational Fibers
Connect areas in the same hemisphere
Allow hemisphere to function as an integrated whole
Superior longitudinal fasciculus
Associational fiber. Connects Wernicke’s and Broca’s areas
Commissural Fibers
interconnect hemispheres. Corpus callosum, anterior and posterior commisures
projection fiers
internal capsule - descending fibers = corticospinal, corticopontine, corticobulbar, ascending fibers = thalamocortico fibers
Pseudobulbar Palsy
UMN lesion to corticobulbar fibers in the internal capsule. (cortical motor neuron axons projecting to cranial nerve motor neurons)
S/S - spastic tongue, hyperreflexic jaw and gag reflexes, slow/slurred speech.
True “bulbar” palsy
would be a lesion to the cranial nerves and would exhibit LMN signs/sxs
Pure motor symptoms CVA
affects the posterior limb of internal capsule, basalar pons or pyramids
Pure sensory symptoms CVA
affects the thalamus or thalamocortical fibers
