Chapter 23 Stroke

Question 1

Define Stroke.

Answer 1

A stroke is defined by the WHO as the rapid development of clinical signs of cerebral dysfunction, with signs lasting at least 24 hours or leading to death with no apparent cause other than that of vascular origin.

Question 2

Name the top 3 causes of death.

Answer 2

Heart disease, cancer, stroke.

Question 3

Describe the classification and subclassifcations of the types of strokes.

Answer 3

The two major types of stroke are ischemic (≈83%) and hemorrhagic (17%).

On further categorizing, 32% are embolic, 31% large vessel thrombotic, 20% small vessel thrombotic, 10% intracerebral hemor-rhagic, and 7% subarachnoid hemorrhagic.

Question 4

Name 3 populations who are at increased risk of developing stroke.

Answer 4

Males, African Americans, and the elderly are at increased risk for developing stroke.

Question 5

Name 3 Modifiable risk factors.

Answer 5

HTN, DM, hyper-cholesterolemia, hyperhomocysteinemia, hypercoagulable states, heart disease, carotid arteriosclerosis, substance abuse, obesity, and a sedentary lifestyle.

Question 6

Name 3 deficits in MCA

Answer 6

Deficits can include c/l hemiplegia/hypesthesia (face and arm worse than leg), c/l homonymous hemianopia, and i/l gaze preference.

Question 7

Describe clinical presentation in dominant hemisphere MCA involvement

Answer 7

receptive aphasia (inferior division of MCA to Wernicke’s area) and/or expressive aphasia (superior division of MCA to Broca’s area) can occur, but classically patients can learn from demonstration and mistakes.

Question 8

What is Gerstmann’s syndrome (parietal lobe)?

Answer 8

MCA. consists of asomatognosia (right–left confusion), dyscalculia, finger agnosia, and dysgraphia.

Question 9

Describe clinical presentation in nondominant hemisphere involvement

Answer 9

spatial dyspraxia and c/l hemineglect may be seen; insight/judgment are often affected (likely to need supervision); ADL recovery is often said to be slower.

Question 10

Name 3 deficits in Acrodermatitis Chronica Atrophican (ACA)

Answer 10

Deficits can include c/l hemiplegia/hypesthesia (leg worse than arm; face and hand spared), alien arm/hand syndrome, urinary incontinence, gait apraxia, abulia (inability to make decisions), perseveration, amnesia, paratonic rigidity (Gegenhalten, or variable resistance to passive ROM), and transcortical motor aphasia (with a dominant hemisphere ACA lesion).

Question 11

Name 5 deficits in Posterior Cerebral Artery (PCA).

Answer 11

Deficits can include c/l homonymous hemianopia, c/l hemianesthesia, c/l hemiplegia, c/l hemiataxia, and vertical gaze palsy.

Question 12

Dominant-sided PCA lesions can lead to what clinical SX?

Answer 12

amnesia, color anomia, dyslexia w/o agraphia, and simultagnosia (defunct perceptual analysis).

Question 13

Nondominant-sided PCA lesions can lead to what clinical SX?

Answer 13

prosopagnosia (cannot recognize familiar faces).

Question 14

The central poststroke pain (Dejerine-Roussy or thalamic pain) syndrome can occur with involvement of what branch of the PCA?

Answer 14

thalamogeniculate branch of the PCA.

Question 15

Name 2 properties of Weber’s syndrome (penetrating branches to the midbrain) (PCA involvement).

Answer 15

i/l CN III palsy and c/l limb weakness).

Question 16

A b/l PCA stroke can cause what 2 syndromes?

Answer 16

Anton syndrome (cortical blindness, with denial) or Bálint’s syndrome, which consists of optic ataxia, loss of voluntary but not reflex eye movements, and an inability to understand visual objects (asimul-tagnosia).

Question 17

The lateral medullary (Wallenberg) syndrome is caused by infarction to what artery?

Answer 17

posterior inferior cerebellar artery

Question 18

Describe the clinical presentation of lateral medullary (Wallenberg) syndrome.

Answer 18

consists of vertigo, nystagmus, dysphagia, dysarthria, dysphonia, i/l Horner’s syndrome, i/l facial pain or numbness, i/l limb ataxia, and c/l pain and temporary sensory loss.

Question 19

The “locked-in” syndrome is due to infarction to what artery? What is system is spared?

Answer 19

basilar artery. b/l pontine infarcts affecting the corticospinal and bulbar tracts, but sparing the reticular activating system. Patients are awake and sensate, but paralyzed and unable to speak. Voluntary blinking and vertical gaze may be intact.

Question 20

What is Anton syndrome?

Answer 20

The Anton syndrome (basilar artery) is characterized by cortical blindness with denial.

Question 21

What cranial nerves are affected in Millard-Gubler syndrome?

Describe the clinical SX of Millard-Gubler syndrome.

Answer 21

Millard-Gubler syndrome is a unilateral lesion of the ventrocaudal pons that may involve the basis pontis and the fascicles of cranial nerves VI and VII.

Symptoms include contralateral hemiplegia, ipsilateral lateral rectus palsy, and ipsilateral peripheral facial paresis. When the penetrating branches of the PCA to the midbrain get affected, it could result in Weber syndrome. Symptoms are ipsilateral characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis or hemiplegia.

Question 22

When is IV tissue plasminogen activator (tPA) indicated for acute ischemic stroke?

Answer 22

within 3 hours of symptom onset.

Question 23

Name 3 Contraindications for the use of tPA.

Answer 23

1. Minor stroke symptoms/tPA
2. Head CT positive for blood
3. BP > 185/100 despite medical treatment
4. Coagulopathy
5. Platelets > 100 k
6. Blood sugar 400
7. Stroke/severe brain injury in past 3 months
8. History of IVH, arteriovenous malformation, or aneurysm
9. History of GI or GU bleed in past 30 days
10. Major surgery in past 14 days
11. Seizure at onset of stroke
12. Acute myocardial infarct

Question 24

What is the evidence regarding SC heparin, low-molecular-weight heparin, or heparinoids in treating acute ischemic stroke?

Answer 24

Clinical trials, in general, do not show clear benefits for SC heparin, low-molecular-weight heparin, or heparinoids in the treatment of acute ischemic stroke, but they are recommended for DVT/pulmonary embolism (PE) prophylaxis in the absence of contraindications.
Low-dose ASA (160 to 325 mg) is recommended within 48 hours for patients with acute ischemic strokes not receiving thrombolytics or anti-coagulation. ASA can be safely used with low-dose SC heparin for DVT prophylaxis.

Question 25

In general, elevated BPs in the acute period should not be aggressively managed EXCEPT in which 2 cases?

Answer 25

mean arterial BP (which is (SBP + 2DBP)/3) > 130 or SBP > 220 mm Hg.

Question 26

Name 3 risk factors for stroke.

Answer 26

Smoking, HTN, hypercholesterolemia.

Question 27

For noncardioembolic cerebral ischemic events (strokes or transient ischemic attacks [TIAs]), one of the three following long-term prophylactic options is recommended. Name these 3.

Answer 27

1. ASA 50 to 325 mg qd;
2. ASA 25 mg bid + extended-release dipyridamole 200 mg bid (Aggrenox);
3. Clopidogrel (Plavix) 75 mg qd (acceptable for ASA-allergic patients).

Question 28

For cardioembolic cerebral ischemic events, oral anticoagulation with what target INR is warranted?

Answer 28

INR of 2.5 (range 2.0 to 3.0) is recommended. INRs > 3.0 are associated with a higher risk of brain hemorrhage that outweighs the potential benefits.

Question 29

Name 3 causes of death post-Stroke.

Answer 29

The major causes of death poststroke are the stroke itself (i.e., progressive cerebral edema and herniation), pneumonia, cardiac disease, and PE.

Question 30

Name 3 complications during the post-Acute Stroke period.

Answer 30

Complications noted during the postacute stroke rehabilitation period include pneumonia and pulmonary aspiration (51% to 78%), falls (22% to 73%), urinary incontinence (37% to 79%), DVT (up to 45%), musculoskeletal pain, and central poststroke pain.

Question 31

Name 3 strategies for treating Urinary Incontinence.

Answer 31

Treatment can include timed-voiding, fluid intake regulation, and treatment of UTIs.
Urinary incontinence typically improves but may still be present in 15% to 20% after 6 months.

Question 32

Name 1 cause of post-Stroke shoulder pain. Name 2 treatments.

Answer 32

Glenohumeral subluxation, seen in 30% to 50% of patients, may play a role in poststroke shoulder pain.4 Arm trough or lapboard use while sitting, stretching of the shoulder depressors/internal rotators, and avoiding pulling on the affected arm during transfers can be key aspects of management during the early rehabilitation phase. If spasticity becomes severe, a subscapularis phenol/botulinum toxin injection can sometimes be helpful.

Question 33

Who gave the first systematic clinical description (In particular, tone and “stereotypic” movements) of motor recovery following stroke?

Answer 33

Twitchell

Question 34

Describe the motor control return pattern.

Answer 34

Motor control returned proximally before distally and LEx function recovered earlier and more completely than UEx function.

Question 35

Who termed “synergy”?

Answer 35

Brunnstrom

Question 36

Name 3 Poor prognostic indicators of post-Stroke recovery.

Answer 36

severe proximal spasticity, proprioceptive facilitation response not present by 9 days, onset of movement at >2 to 4 weeks, absence of voluntary hand movement at 4 to 6 weeks, or a prolonged flaccid period.

Question 37

Post-Stroke Full recovery, when it occurred, was usually complete within what time frame?

Answer 37

12 weeks

Question 38

Brunnstrom later formalized the stages of motor recovery. What are these stages?

Answer 38

1. Flaccid limb
2. Some spasticity with weak flexor and extensor synergies
3. Prominent spasticity; voluntary motion occurs within synergy patterns
4. Some selective activation of muscles outside of synergy patterns. Spasticity reduced
5. Most limb movement independent from limb synergy; spasticity further reduced but still present with rapid movements
6. Near-normal coordination with isolated movements
7. Restoration to normal

Question 39

What is the most commonly used approach for post-Stroke rehabilitation?

Answer 39

Neurodevelopmental approach/Bobath approach

Question 40

What is the goal of the Neurodevelopmental approach/Bobath approach? What is it’s opposite?

Answer 40

The most commonly used approach (“hands-on” approach, touch and pressure applied by therapist).
The goal is to normalize tone, inhibit primitive patterns of movement, and facilitate selective automatic, voluntary reactions and subsequent normal patterns.
Suppress abnormal muscle patterns, which is contradictory to Brunnstrom’s approach. Proximal key points include shoulders and pelvis; distal key points include upper and lower extremities (typically the hands and feet).
Focuses on the relationship between sensory input and motor output.

Question 41

What is the goal of Proprioceptive neuromuscular facilitation (PNF)?

Answer 41

It is often a combination of passive stretching and isometric contractions.
Uses spiral and diagonal components of movement with the goal of facilitating movement patterns that will have more functional relevance than the traditional technique of strengthening individual group muscles.
Resistance is used during spiral and diagonal movement patterns with the goal of facilitating irradiation of impulses to other parts of the body associated with the primary movement.

Question 42

What is the goal of the Brunnstrom approach?

Answer 42

Uses primitive synergistic patterns in training in an attempt to improve motor control through central facilitation.
Synergies and primitive refluxes are considered normal processes of recovery.
Enhances specific synergies through the use of cutaneous proprio-ceptive stimuli and central facilitation using Twitchell’s recovery.

Question 43

What is the goal of the Rood approach/sensorimotor approach?

Answer 43

Uses sensorimotor stimulation to modify muscle tone and voluntary motor activity.
Inhibitory or facilitatory input through the use of quick stretching, icing, fast brushing, slow stroking, tendon tapping, and vibration and joint compression to promote contraction of proximal muscles.

Question 44

What is the goal of the Constraint-induced movement therapy?

Answer 44

Constraint-induced movement therapy (CI or CIMT) is a technique pioneered by UAB behavioral neuroscientist Edward Taub.
Requires the patient to be able to extend their wrist and fingers.
The focus of CI lies in forcing the patient to use the affected limb by restraining the unaffected one. The affected limb is then used intensively for either 3 or 6 hours a day for at least 2 weeks.

Question 45

What is the most consistent predictor of discharge post-Stroke and post-admission to acute rehabilitation?

Answer 45

Admission functional ability is the strongest and most consistent predictor of discharge.

Question 46

What 2 properties are significant predictors of functional status at the time of discharge from acute rehabilitation for post-Stroke?

Answer 46

admission functional status score and onset admission interval.

Question 47

There is evidence of better functional prognosis in stroke survivors with what type of stroke?

Answer 47

hemorrhagic stroke (better than ischemic stroke)

Question 48

Approximately 80% of stroke survivors walk by what time frame?

Answer 48

a year following stroke

Question 49

Why is motor rehabilitation important post-Stroke?

Answer 49

earlier and more intensive mobilization after stroke may fast-track return to unassisted walking and improve functional recovery

Question 50

The best neurologic recovery is seen by what time frame?

Answer 50

11 weeks for 95% of patients

Question 51

Most ADL recovery (by Barthel Index) is by what time frame? Recovery can take up to how long?

Answer 51

12.5 weeks with daily PT/OT, but recovery could take 2 years or more.