Flashcards in Chapter 23 Stroke Deck (51):
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.
Name the top 3 causes of death.
Heart disease, cancer, stroke.
Describe the classification and subclassifcations of the types of strokes.
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.
Name 3 populations who are at increased risk of developing stroke.
Males, African Americans, and the elderly are at increased risk for developing stroke.
Name 3 Modifiable risk factors.
HTN, DM, hyper-cholesterolemia, hyperhomocysteinemia, hypercoagulable states, heart disease, carotid arteriosclerosis, substance abuse, obesity, and a sedentary lifestyle.
Name 3 deficits in MCA
Deficits can include c/l hemiplegia/hypesthesia (face and arm worse than leg), c/l homonymous hemianopia, and i/l gaze preference.
Describe clinical presentation in dominant hemisphere MCA involvement
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.
What is Gerstmann's syndrome (parietal lobe)?
MCA. consists of asomatognosia (right–left confusion), dyscalculia, finger agnosia, and dysgraphia.
Describe clinical presentation in nondominant hemisphere involvement
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.
Name 3 deficits in Acrodermatitis Chronica Atrophican (ACA)
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).
Name 5 deficits in Posterior Cerebral Artery (PCA).
Deficits can include c/l homonymous hemianopia, c/l hemianesthesia, c/l hemiplegia, c/l hemiataxia, and vertical gaze palsy.
Dominant-sided PCA lesions can lead to what clinical SX?
amnesia, color anomia, dyslexia w/o agraphia, and simultagnosia (defunct perceptual analysis).
Nondominant-sided PCA lesions can lead to what clinical SX?
prosopagnosia (cannot recognize familiar faces).
The central poststroke pain (Dejerine-Roussy or thalamic pain) syndrome can occur with involvement of what branch of the PCA?
thalamogeniculate branch of the PCA.
Name 2 properties of Weber's syndrome (penetrating branches to the midbrain) (PCA involvement).
i/l CN III palsy and c/l limb weakness).
A b/l PCA stroke can cause what 2 syndromes?
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).
The lateral medullary (Wallenberg) syndrome is caused by infarction to what artery?
posterior inferior cerebellar artery
Describe the clinical presentation of lateral medullary (Wallenberg) syndrome.
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.
The “locked-in” syndrome is due to infarction to what artery? What is system is spared?
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.
What is Anton syndrome?
The Anton syndrome (basilar artery) is characterized by cortical blindness with denial.
What cranial nerves are affected in Millard-Gubler syndrome?
Describe the clinical SX of Millard-Gubler syndrome.
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.
When is IV tissue plasminogen activator (tPA) indicated for acute ischemic stroke?
within 3 hours of symptom onset.
Name 3 Contraindications for the use of tPA.
1.Minor stroke symptoms/tPA
2.Head CT positive for blood
3.BP > 185/100 despite medical treatment
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
What is the evidence regarding SC heparin, low-molecular-weight heparin, or heparinoids in treating acute ischemic stroke?
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.
In general, elevated BPs in the acute period should not be aggressively managed EXCEPT in which 2 cases?
mean arterial BP (which is (SBP + 2DBP)/3) > 130 or SBP > 220 mm Hg.
Name 3 risk factors for stroke.
Smoking, HTN, hypercholesterolemia.
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.
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).
For cardioembolic cerebral ischemic events, oral anticoagulation with what target INR is warranted?
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.
Name 3 causes of death post-Stroke.
The major causes of death poststroke are the stroke itself (i.e., progressive cerebral edema and herniation), pneumonia, cardiac disease, and PE.
Name 3 complications during the post-Acute Stroke period.
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.
Name 3 strategies for treating Urinary Incontinence.
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.
Name 1 cause of post-Stroke shoulder pain. Name 2 treatments.
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.
Who gave the first systematic clinical description (In particular, tone and “stereotypic” movements) of motor recovery following stroke?
Describe the motor control return pattern.
Motor control returned proximally before distally and LEx function recovered earlier and more completely than UEx function.
Who termed “synergy”?
Name 3 Poor prognostic indicators of post-Stroke recovery.
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.
Post-Stroke Full recovery, when it occurred, was usually complete within what time frame?
Brunnstrom later formalized the stages of motor recovery. What are these stages?
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
What is the most commonly used approach for post-Stroke rehabilitation?
Neurodevelopmental approach/Bobath approach
What is the goal of the Neurodevelopmental approach/Bobath approach? What is it's opposite?
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.
What is the goal of Proprioceptive neuromuscular facilitation (PNF)?
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.
What is the goal of the Brunnstrom approach?
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.
What is the goal of the Rood approach/sensorimotor approach?
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.
What is the goal of the Constraint-induced movement therapy?
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.
What is the most consistent predictor of discharge post-Stroke and post-admission to acute rehabilitation?
Admission functional ability is the strongest and most consistent predictor of discharge.
What 2 properties are significant predictors of functional status at the time of discharge from acute rehabilitation for post-Stroke?
admission functional status score and onset admission interval.
There is evidence of better functional prognosis in stroke survivors with what type of stroke?
hemorrhagic stroke (better than ischemic stroke)
Approximately 80% of stroke survivors walk by what time frame?
a year following stroke
Why is motor rehabilitation important post-Stroke?
earlier and more intensive mobilization after stroke may fast-track return to unassisted walking and improve functional recovery
The best neurologic recovery is seen by what time frame?
11 weeks for 95% of patients