Neuro Pathology Pt. 1 Flashcards

Stroke, Cerebellum lesions, MS, & Parkinson's Disease (PD)

1
Q

Define a stroke

A
  • Occurs when the blood supply to the brain is interrupted or reduced
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2
Q

Define an ischemic stroke

A
  • Makes up 80% of cases
  • Cerebral thrombosis: formation or development of a blood clot or thrombus within the cerebral arteries or their branches
  • Cerebral embolism: traveling bits of matter that produce occlusion & infarction in the cerebral arteries
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3
Q

Define a hemorrhagic stroke

A
  • Abnormal bleeding as a result of rupture of a blood vessel
  • Occurs in about 20% of cases
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4
Q

Define a TIA (transient ischemic attack)

A
  • A temporary period of symptoms resulting from decrease blood supply to the brain
  • Precursor to major stroke; lasts <24hrs
  • No permanent damage
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5
Q

Risk factors for a stroke

A
  • Atherosclerosis
  • HTN
  • Cardiac disease
  • DM, metabolic syndrome
  • TIAs
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6
Q

What are the 4 after effects/pathophysiology of a stroke

A
  • Cerebral anoxia: lack of O2 supply to the brain (irreversible damage begins after 4-6 min)
  • Cerebral infarction: irreversible cellular damage
  • Cerebral edema: accumulation of fluids within brain causes further dysfunction, elevates ICP, can result in herniation & death
  • Secondary cell death: death of neurons around the specific area of damage
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7
Q

Characteristics of a MCA stroke

A
  • UEs affected more than LEs
  • Contralateral hemiplegia of face
  • Contralateral hemisensory loss
  • Homonymous hemianopsia
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8
Q

Characteristics of a ICA (internal carotid artery) syndrome stroke

A
  • ICA comes off the common carotid artery and gives off an ophthalmic branch and terminates in the ACA (anterior cerebral artery)
  • Has signs and symptoms similar to MCA involvement with reduced levels of consciousness
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9
Q

Characteristics of an ACA stroke

A
  • LEs affected more than UEs
  • Contralateral hemiplegia
  • Contralateral hemisensory loss
  • Urinary incontinence
  • Problems with bimanual tasks
  • Apraxia (inability to perform particular purposeful actions)
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10
Q

Characteristics of a PCA stroke

A
  • Contralateral sensory loss
  • Involuntary movements: choreoathetosis, tremor, hemiballismus
  • Transient contralateral hemiparesis
  • Homonymous hemianopsia
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11
Q

Characteristics of an internal capsule lesion posterior limb stroke

A
  • Lacunar (pure motor) stroke
  • Contralateral hemiplegia UE and LE
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12
Q

Describe the different types of vertebrobasilar artery syndrome

A
  • Medial medullary syndrome: occlusion of the vertebral anterior branch of the lower basilar artery
  • Lateral medullary (Wallenberg’s) syndrome: occlusion of vertebral, posterior inferior cerebellar, or basilar artery
  • Basilar artery syndrome: occlusion at the level of the pons; locked-in syndrome
  • Medial inferior pontine syndrome: occlusion of the paramedic branch of basilar artery
  • Lateral inferior pontine syndrome: occlusion of the anterior inferior cerebellar artery (AICA)
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13
Q

Characteristics of a midbrain stroke

A
  • Contralateral hemiplegia
  • Possible contralateral CN III palsy
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14
Q

Characteristics of a medial pontine syndrome stroke

A
  • Ipsilateral: nystagmus, cerebellar ataxia, paralysis of conjugate gaze to side of lesion, diplopia
  • Contralateral: hemiparesis UE/LE, impaired sensation
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15
Q

Characteristics of a lateral pontine syndrome (AICA) stroke

A
  • Ipsilateral: ataxia, nystagmus, vertigo, facial paralysis, paralysis of conjugate gaze to the side of the lesion, deafness, tinnitus, impaired facial sensation
  • Contralateral: impaired pain & temperature sensation half of body
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16
Q

Characteristics of a medial medullary syndrome stroke

A
  • Ipsilateral: paralysis of half of tongue
  • Contralateral: hemiplegia UE/LE, impaired sensation
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17
Q

Characteristics of a lateral medullary (Wallenberg’s) syndrome stroke

A
  • Ipsilateral: ataxia, nystagmus, vertigo, loss of pain & temperature to face, sensory loss UE/trunk/LE
  • Contralateral: loss of pain & temperature to body & face
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18
Q

What parts of the brain are involved in a pure sensory lacunar stroke

A
  • Involvement of the ventrolateral thalamus or thalamocortical projections
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19
Q

What parts of the brain are involved in a dysrthria/clumsy hand syndrome stroke

A
  • Involving the base of the pons, genu of anterior limb, or the internal capsule
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20
Q

What parts of the brain are involved in a ataxic hemiparesis stroke

A
  • Involving the pons, genu of internal capsule, corona radiata, or cerebellum
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21
Q

What are the 6 sequential recovery stages of a stroke

A
  • Stage 1: initial flaccidity, no voluntary movement
  • Stage 2: emergence of spasticity, hyperreflexia, synergies (mass patterns of movement)
  • Stage 3: voluntary movement possible, but only in synergies; spasticity strong
  • Stage 4: voluntary control in isolated joint movements emerging, corresponding decline of spasticity & synergies
  • Stage 5: increasing voluntary control out of synergy; coordination deficits present
  • Stage 6: control & coordination near normal
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22
Q

Behaviors of a left hemisphere lesion (right hemiplegia)

A
  • Slow
  • Cautious
  • Hesitant
  • Insecure
  • Often aware of their impairments resulting in frustration
  • Aphasia
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23
Q

Behaviors of a right hemisphere lesion (left hemiplegia)

A
  • Impulsive
  • Quick
  • Indifferent
  • Often exhibit poor judgement & safety, overestimating their abilities while understanding their problems
  • Perceptual deficits
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24
Q

Describe the components of an UE flexion synergy

A
  • Scapular retraction/elevation
  • Shoulder abduction, ER
  • Elbow flexion
  • Forearm supination
  • Wrist and finger flexion
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25
Q

Describe the components of an UE extension synergy

A
  • Scapular protraction
  • Shoulder adduction, IR
  • Elbow extension
  • Forearm pronation
  • Wrist and finger flexion
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26
Q

Describe the components of an LE flexion synergy

A
  • Hip flexion, abduction, ER
  • Knee flexion
  • Ankle DF/inversion
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27
Q

Describe the components of an LE extension synergy

A
  • Hip extension, adduction, IR
  • Knee extension
  • Ankle PF/inversion
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28
Q

What are some typical gait deficits in stroke patients

A
  • Retracted/flexed hip
  • Trendelennburg limp
  • Scissoring
  • Insufficient pelvic rotation during swing
  • Circumduction
  • Knee hyperextension
  • Footdrop
  • Unequal step lengths
  • Decreased cadence, uneven timing
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29
Q

Key red flags/PT implications for stroke patients

A
  • Avoid traction or overhead activity when pts have flaccid shoulder muscles with risk of subluxation/dislocation
  • Emphasize compensation strategies for pts with sensory & perceptual losses to prevent additional injury & functional losses
  • Monitor HR and BP closely during exercise or activity training; monitor for signs?symptoms of cardiovascular compromise
30
Q

Common outcome measures used/specific for stroke patients

A
  • Fugl-Meyer assessment of motor performance
  • Functional independence measure (FIM): motor & cognitive tasks
  • Postural assessment scale for stroke patients
  • Trunk impairment scale
  • Stroke impact scale: self report
31
Q

Interventions for stroke patients

A
  • Promote active problem solving independence
  • Focus one goal directed tasks
  • Compensatory strategies
  • Improve cardiopulmonary endurance & aerobic conditioning
  • BWS (body weight support) and motorized treadmill training
  • Constraint induced movement therapy (CIMT)
  • AFO
  • FES (functional electrical stimulation)
32
Q

Common drugs and their purpose used for strokes

A
  • t-PA: indicated for acute ischemic stroke; monitor BP
  • Baclofen, Tizanidine, Dantrolene sodium (anti-spasticity): indicated to relax skeletal muscle/anti-spasticity; fall risk, monitor functional ability & limitations
  • Diazepam: indicated for anti-spasticity, seizure prevention; fall risk, reduced psychomotor ability
  • Botulinum (botox): indicated for local relief of muscle tone & spasms; rare systemic effects including generalized weakness, flaccidity, difficulty speaking, dysphagia, and/or respiratory distress
33
Q

How to promote learning in left hemisphere lesions (right hemiplegia)

A
  • Develop an appropriate communication base: words, gestures, pantomime; assess level of understanding
  • Give frequent feedback & support
  • Do not underestimate ability to learn
34
Q

How to promote learning in right hemisphere lesson (left hemiplegia)

A
  • Use verbal cues; demonstrations or gestures may confuse pts with visuospatial deficits
  • Give frequent feedback: focus on slowing down & controlling movement
  • Focus on safety
  • Avoid environmental clutter
  • Do not overestimate ability to learn
35
Q

What are the 4 types of primary brain injury for a TBI

A
  • Diffuse axonal injury: disruption/tearing of axons & small blood vessels
  • Focal injury: contusions, lacerations, mass effect from hemorrhage, & edema
  • Coup-contracoup: injury at point of impact & opposite point of impact
  • Closed or open injury: with fracture of the skull
36
Q

What are the secondary brain damage to TBI

A
  • Hypoxic-ischemic injury: results from systemic problems that compromise cerebral circulation
  • Swelling/edema: can cause mass effect with increased ICP, brain herniation, & death
  • Electrolyte imbalance and mass release of damaging neurotransmitters
37
Q

Define a concussion

A
  • Loss of consciousness either temporary or permanent resulting from injury or blow to head with impaired functioning of the brainstem reticular activating system (RAS)
  • May see changes in HR, BP, & RR
38
Q

What re the CPG recommendations for AFO/FES use post-stroke

A
  • Chronic FES: increase tibialis anterior activation, improve dynamic balance, improve walking endurance, improve mobility, improve gait speed
  • Acute FES: improve mobility
  • Chronic AFO: improve gait speed, mobility, walking endurance, dynamic balance, QoL for footdrop
  • Acute AFO: improve gait speed
39
Q

What are the recovery stages from diffuse axonal injury

A
  • Coma: unable to arouse
  • Unresponsive wakefulness syndrome/vegetative state: return of sleep/wake cycles
  • Mute responsiveness/minimally responsive: pt shows signs of fluctuating awareness
  • Confusional state: all cognitive operations are affected; pt is unable to form new memories
  • Emerging independence: some memory possible, frequently uninhibited social behaviors
  • Intellectual/social competence: increasing independence although cognitive difficulties persist along with behavior/social problems
40
Q

Describe a signs/symptoms of a mild TBI

A
  • LOC ≤30 min
  • Alteration of consciousness is brief; >24hrs
  • Posttraumatic amnesia <1 day
  • Glasgow Coma Scale 13-15
  • Imaging is normal
41
Q

Describe a signs/symptoms of a moderate TBI

A
  • LOC >30 min but <24hrs
  • Alteration of consciousness >24hrs
  • Posttraumatic amnesia 1-7 days
  • Glasgow coma scale 9-12
  • Imaging can be normal or abnormal
42
Q

Describe a signs/symptoms of a severe TBI

A
  • LOC >24hrs
  • Alteration of consciousness >24hrs
  • Posttraumatic amnesia >7 days
  • Glasgow coma scale <9
  • Imaging can be normal or abnormal
43
Q

Outcome measures recommended for TBI

A
  • Functional Independence Measure (FIM)
  • Rancho’s Levels of Cognitive Functioning (LOCF)
  • Coma Recovery Scale
  • Agitated Behavior Scale
  • Mass Attention Rating Scale
  • Modified Ashworth Scale
  • Action Research Arm Test (ARAT)
  • High Level Mobility Assessment (Hi-mat)
  • Community Balance & Mobility Scale
  • Dizziness Handicap Inventory (DHI)
  • Community Integration Questionnaire
44
Q

What are the levels of the Rancho’s Levels of Cognitive Function (LOCF)

A
  • I: no response
  • II: Generalized response
  • III: Localized response
  • IV: confused, agitated response
  • V: confused, inappropriate, non agitated response
  • VI: confused, appropriate response
  • VII: automatic, appropriate response
  • VIII: purposeful, appropriate response
45
Q

Define sympathetic storming and what to examine for

A
  • The result of hypothalamic stimulation of the SNS with an increase in circulating corticoids & catecholamines (stress response)
  • Examine for alterations in LOC, increased posturing, dystonia, HTN, hyperthermia, tachycardia, tachypnea, diaphoresis, & agitation
46
Q

Common drugs used for TBI/SCI management

A
  • Baclofen, Tizanidine, Dantrolene sodium: relax skeletal muscle, anti-spasticity
  • Diazepam: anti-spasticity, seizure prevention
  • Botulinum toxin (Botox): local relief of muscle tone & spasms
  • Carbamazepine, Gabapentin, Pregabalin: seizure prevention, spasticity (gabapentin); fall risk, monitor seizure Hx, functional ability, & limitations
47
Q

Concussion signs observed

A
  • Appears dazed or stunned
  • Can’t recall events prior to or after a hit/fall
  • Forgets an instruction, appears confused
  • Moves clumsily
  • Answers questions slowly
  • Loses consciousness
  • Shows mood, behavior, or personality changes
48
Q

Concussion symptoms reported

A
  • HA or pressure in head
  • Nausea or vomiting
  • Balance problems, dizziness, blurry vision
  • Bothered by light or noise
  • Feeling sluggish, hazy, foggy, or groggy
  • Confusion, concentration or memory problems
  • Just not “feeling right” or “feeling down”
49
Q

Seek immediate emergency care if the adult or child experiences any of the following after a blow/hit to the head (possible TBI)

A
  • Drowsiness or inability to wake up
  • One pupil larger than the other
  • Repeat vomiting or nausea, convulsions, or seizures
  • LOC lasting longer than 30 secs
  • HA that gets worse over time
  • Slurred speech, numbness, or decreased coordination
  • Changes in behavior: irritability, restlessness, agitation
  • Confusion, disorientation, or amnesia
50
Q

Describe second impact syndrome

A
  • A 2nd concussion is experienced before the brain has a chance to heal from the first event
51
Q

Describe post concussion syndrome

A
  • Persistent post concussion symptoms lasting ≥3 months
  • Symptoms may include post-traumatic seizures, increased risk of depression, and mild-cognitive impairment later in life
52
Q

Define chronic traumatic encephalopathy (CTE)

A
  • A progressive neurodegenerative brain disease resulting form repetitive head trauma
  • Seen in athletes & boxers with a Hx of multiple concussions & repeated head injury
53
Q

Level A evidence for examination and treatment of concussion/mild TBI

A
  • Assess Dix-Hallpike test or other appropriate positional test(s)
  • Use carnality repositioning intervention for vestibulo-oculomotor impairments
  • Provide symptom guided, progressive, aerobic exercise training program
54
Q

Typical signs and symptoms of chronic traumatic encephalopathy (CTE)

A
  • Recurrent HA and dizziness
  • Cognitive impairments: memory loss, difficulty thinking, planning, & carrying out tasks eventually progressing to dementia
  • Mood or behavioral disturbances
  • Impaired judgement & impulse control, aggression, irritability, anger
  • Movement disorders (late)
55
Q

Signs and symptoms of epilepsy

A

-Altered consciousness
- Altered motor activity (convulsion): tonic - stiffening & rigidity or muscles; clonic - rhythmic jerking or extremities
- Sensory phenomena
- Autonomic phenomena: sudden attack of anxiety, tachycardia, sweating, abnormal sensation rising up in upper abdomen & chest
- Cognitive phenomena: sudden failure of comprehension, inability to communicate, hallucinations

56
Q

Describe a grand mal/generalized seizure

A
  • All areas of brain are involved
  • Dramatic LOC with stiffening then rhythmic movements of arms/legs
  • Eyes are generally open
  • Altered breathing
  • Loos of urine
  • Typically lasts 2-5 minutes
57
Q

Describe an absence/petit mal seizure

A
  • Posture is maintained
  • Repetitive blinking or other small movements may be present
  • Typically brief only lasts a few seconds
  • Can occur multiple times throughout the day
58
Q

Describe a partial/focal seizure

A
  • Only one part of the brain is involved
  • Symptoms are focal (specific are of the body)
59
Q

Define status epilepticus

A
  • Prolonged seizure or a series of seizures (lasting >30 minutes) with very little recovery between attacks
  • May be life threatening
  • Medical emergency
60
Q

Signs and symptoms of a vestibulocerebellar/flocculonodular lobe (archicerebellum) lesion

A
  • Ocular dysmetria
  • Poor smooth pursuit
  • Dysfunctional vestibulo-ocular reflex (VOR)
  • Impaired eye/hand coordination
  • Gait/trunk ataxia
  • Little change in tone or dyssynergia or extremity movements
61
Q

Signs and symptoms of a spinocerebellum/rostral cerebellum/anterior lobe (paleocerebellum) lesion

A
  • Hypotonia with weakness/fatigue
  • Truncal ataxia: dysequilibrium, static postural tremor, high guard arm position
  • Ataxic gait: unsteady, increased falls
62
Q

Signs and symptoms of a hemisphere/posterior lobe (neocerebellum) lesion

A
  • Intention tremor
  • Dysdiadochokinesia: impaired RAM
  • Dysmetria: overshooting, errors of force, direction, amplitude
  • Dyssynergia: abnormal timing of movement (errors in onset, stop, and velocity)
63
Q

General signs and symptoms of a cerebellum lesion

A
  • Asthenia: generalized weakness (3-4/5 MMT)
  • Hypotonia: difficulty with postural control of proximal (axial) muscles
  • Motor learning impairments: decreased anticipatory control, feedback, & learning delays
  • Cognition deficits in info procession, attention deficits
  • Emotional dysregulation: changes in emotional behaviors
64
Q

What kind of motor learning strategy is useful in treatment of patients with a cerebellum lesion

A
  • Low-stimulus environment (closed environment) ideal
  • Focus on practice & repetition
  • Distributed practice (endurance may be low)
65
Q

Describe multiple sclerosis (MS)

A
  • Chronic, progressive, demyelinating disease of the CNS affecting mostly young adults (20-50 yrs)
  • Female affected more than males
  • Characterized by demyelinating lesions (plaques) with variable symptoms
  • Exacerbating factors include infections, trauma, pregnancy, and stress
66
Q

Things that cause transient worsening of MS symptoms

A
  • Adverse reactions to heat
  • Hyperventilation
  • Dehydration
  • Fatigue
67
Q

What re the 4 types of MS

A
  • Relapsing remitting: discrete attacks of neurological deficits with either full/partial recovery (85% of cases); lack of disease progression when in remission
  • Primary progressive: disease progression & a deterioration in function from onset
  • Secondary progressive: initial relapsing-remitting course followed by a change to a progressive course with a steady decline in function
  • Progressive relapsing: steady deterioration in disease from onset but with occasional acute attacks; continuation of disease progression when in remission
68
Q

Define clinically isolated syndrome (CIS) for MS

A
  • 1st episode of inflammatory demyelination in the CNS that could become MS if additional activity occurs; can progress to relapse remitting MS
69
Q

What re 2 common causes of death in MS patients

A
  • Urinary tract infection (UTI)
  • Respiratory infection
70
Q

Classic signs and symptoms of Parkinson’s disease (PD)

A
  • Rigidity (leadpipe or cogwheel)
  • Bradykinesia (hypokinesia/slow movements)
  • Resting tremor
  • Impaired postural reflexes
71
Q

What are the 5 stages of PD (Hoehn and Yahr classification)

A
  • I: minimal or absent disability, unilateral symptoms
  • II: minimal bilateral or midline involvement, no balance involvement
  • III: impaired balance, some restrictions in activity
  • IV: all sx present & severe, stands & walks only with assistance
  • V: confinement to bed or wheelchair
72
Q

Pharmacology for Parkinson’s disease

A
  • Levodopa & Carbidopa: help with PD motor sx
  • COMT inhibitors (Catecholo-Methyl Transferase): prolongs levodopa effects
  • Dopamine agonists: may slow early disease progression
  • Anticholinergics: help control tremors, rigidity, & dystonia
  • Amantadine: enhances dopamine release
  • Monoamine Oxidase inhibitor (MAO)/Selegiline: increases dopamine; used during early disease to slow progression