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Neurological and Medical Complication of Stroke
Harvey A. Drapkin, D.O. F.A.C.N.
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Stroke is the third leading cause of death as well as the third leading cause of disability
in the United States.
Approximately 700,000 per year and
160,000 fatalities.
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Mortality Predictors Include
Stroke severity; but older age, concomitant medical diseases, and recurrent stroke are also associated with poor short-term prognosis.
Condition is worsened by neurological and medical complications in up to 80% of patients.
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Mortality Causes
• Week One – 90% of deaths are due directly to the Infarct (Edema, Extension, Herniation)
• Weeks 2-4 – Pulmonary Embolism is most common cause of death and risk remains high for 3 months
• Weeks 8-12 – Bronchopneumonia. Later Heart Disease.
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Slide of Cerebral Infarct with Edema
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Slide of Cerebral Infarct with Edema
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Treatment of Increased Intracranial Pressure
• Osmotic Agents
• Hyperventilation
• External Ventricular Drainage
Hypoxia, Hypercapnia and Hyperthermia must be avoided.
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Treatment of I I P
• Moderate hypothermia (32-34º) – May be helpful
• Hemicraniectomy and Duroplasty – Supratentorial
• Cerebellectomy and/or Evacuation/Decompression
Generally younger patient – better outcome.
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Seizures and Stroke
Seizures at onset – often partial, may represent 4.4% of stroke patients. S.E. – 1%
Early seizures after stroke – within days 3-6%
Late seizures after stroke – after 14 days, more likely to recur without AED treatment.
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Seizures and Stroke
More frequent occurrence in:
• Severe disabling stroke
• Hemorrhagic Strokes
• Stroke with Cortical Involvement
Stroke – Most common etiology for S.E. in Elderly.
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Seizures and Stroke
Who to treat and how long?
One way is to exclude other causes for seizure, i.e. Hypoxia, Hypoglycemia, etc. and start AED’s
Most Neurologists treat for 2-3 years
EEG – Beneficial especially in Non Convulsive S.E.
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Stroke and Seizure
• Do seizures affect stroke outcome? Yes.
“Prolonged focal motor seizure often cause worsening of the previous motor deficit” Bogousslauskt, et al.
• Which drugs – Classical or new?
Either but consider drug interactions of “classicals”, i.e. Warfarin.
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DVT’s, VTE’s and Pulmonary Emboli
• One study of patients with stroke and confirmed P.E. showed that 50% of patients had sudden death
• Diagnosis of VTE is complicated by the stroke and its impairment. Noninvasive testing often very helpful
• Tx with Heparin/Warfarin – risk of bleed, death, etc. 3%.
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Blood Pressure – ASA Guidelines
• High or Low may affect stroke outcome
• Early stage – systolic BP 150-170 is optimal
• More aggressive Tx with malignant HTN Myocardial Ischemia, Aortic Dissection, post TPA
• LBP – often Hypovolemia & Tx with Fluids, pressors PRN
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Management of Med. & Neurol. Complications
Prevention (pathways, standard orders, etc.)
Diagnosis (index of suspicion, diagnostic, modalities)
Treatment (general and complication specific)
Care and outcomes are best with specialized multi-disciplinary stroke unit.
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Hyperglycemia and Stroke
• Blood glucose elevated in 40-50% of patients in the first 24 hours. Over half are not D.M.
• Insulin Tx reduces infarct size and improves prognosis (benefits focal & global brain ischemia)
• Aim to maintain normal glucose and avoid poor outcome.
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Infections and Fever in Stroke
• In acute stage of stroke are associated with increased fatalities and poor functional outcomes.
• Each degree of Celsius doubles risk of poor outcome.
• Pneumonia – in 20-30% of patients. 25% of deaths in first month
• UTI’s common, moderate Hypothermia may be helpful
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Cardiac Abnormalities in Stroke
• One-third of patients – ST Segment Depression or Ventricular Arrhythmias – first 5 days
• Previously undiagnosed Arrhythmias including A-Fib – seen in 50%
• Insular Cortex Lesions predispose to EKG changes Arrhythmias and sudden death. Rec-24-48 hour monitor and treatment.
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Emotional Disturbances after Stroke
• Anosognosia – neglect of perceptual loss
• 33% of patients have poor or no memory of acute event
• Can occur without specific damage to “Learning Structures”
• Partly explains delay in seeking medical care, compared to heart patients.
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Emotional Disturbances after Stroke
• Acute Phase includes: overt sadness 72%, disinhibition 56%, lack of adaption 44%, environmental withdrawal 40%, crying 27%, anosognosia & passivity 24%, aggressiveness 11%
• Left and Right brain affected
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Emotional Disturbances after Stroke
Catastrophic reaction – occurs in 3%.
Strong correlation with aphasia and with left insular location. 66% of these patients develop depression later in chronic stage.
Acute psychosis seen in L. PCA Infarct
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Chronic Phase Emotional Disturbances
Post-Stroke depression – 40% major or minor
Associated with left frontal and B.G. lesions.
Resistance to SSRI’s? Positive thinking affected.
Small vessel disease on MRI – high correlation with PSD-A
Absence of guilt, suicidal ideation, But treat!
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Chronic Phase Emotional Disturbances
• Anxiety disorders – 25% or more
• PTSD – like syndrome – independent of neurological impairment. More frequent in patients with concern of death in acute phase.
• Increased with B.G. stroke. Role in re-experience?
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Chronic Phase-Mania, Bipolar Dx; Psychosis
• Mania related to right hemisphere lesions• Psychosis – rare. May appear as DMS
including reduplicative paramnesia, Capgras’ syndrome, etc.
• Delusional mis-ID syndrome – functional disconnect between past amnesic information and integration with present information
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Chronic Phase – Emotional Hyperactivity & Flattening
• Seen in bilateral Vascular Lesions and Vascular Dementia
• Some have emotional disinhibition, outbursts and loss of emotional control.
• Emotional Flattening – impaired automatic response to emotional valence of stimuli
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Post-Stroke Fatigue
• Multifactorial and common (68%)• Heightened sensation of physical or mental
strain• Contributing factors – T.I.M.E., sleep
disorders, immobility-deconditioning, psychologic.
• Treatments – Pharmacologic and Non-Pharmacologic
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Cognitive Syndrome of Post-Stroke Dementia
• 30% of patients slow progression
• Predominant executive dysfunction
• Affects subcortical and frontal lobes
• Memory and language deficits less obvious
• Late stages - memory deficits and dementia
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Major Risk Factors for Cognitive Impairment
Age – Diabetes Mellitus – Atrial FIB – Ethnicity vs. Educational attainment –
Aphasia – Depression – Previous Stroke – Genetic?
Stroke location and severity
Treat = Cholinergic replacement
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Central Post-Stroke Pain
• Can occur after lesions of spinothalamic pathway and corticopetal projections
• Constant or Intermittent pain post-stroke. Associated with sensory abnormality in the painful area.
• Aberrant neural activity – DEAFF- Facil./Inhib. Imbalance
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Central Post-Stroke Pain
• Begins within first month (63%) – up to 3 years
• Incidence 8% or more. Tx - Resistant
• Tx: Modalities – Antidepressants, anticonvulsants, glutamergic, gabaergic, opiates
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CPSP Treatment – Evidence Based
• Short term pain control – Lidocaine, Propofol, I.V.’s
• 1st line Drugs – Amitriptylline 75mg+, LTG 200mg+
• 2nd line Drugs – Mexilitine up to 10mg/kg/day, Fluvoxamine up to 125mg/day, Gabapentin 1200mg/day or more.
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Sleep and Stroke
• 50% or more have SDB, mostly OSA.
• SDB – poorer long-term outcome, increased mortality.
• SDB – may improve spontaneously. More often requiring CPAP or O₂. Hypnotics, DA agents and stimulants for patients with Thalamic Brainstem Lesions
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Other Complications of Stroke
• Falls, Fractures, Osteoporosis
Prophylactic I.V. Bisphosphonates??
• Voiding and Sexual Dysfunction
Medical – Urological – Rehabilitation – Nursing Team Approach
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Secondary Stroke Prevention
• 200,000 of Total Strokes• Profound effect on Morbidity-Mortality• ABCDE Treatment options
– A – Anti-platelet, Anticoag., Art. Revascularization
– B – Blood pressure control
– C - Cholesterol, Cig. Cessation
– D – Diet
– E – Exercise
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Summary
• Prevention, Diagnosis, and Treatment of Stroke complications can decrease both Morbidity and Mortality.
• Monitor closely for early detection.
• Better outcomes with specialized stroke units.
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Selected References:
1. Annoni, Jean-Marie et al. Emotional Disturbances after Stroke, Clinical and Experimental Hypertension 28:243-249, 2006.
2. Appelros P. et al. Lacunar Infarcts, Functional and Cognitive Outcomes……Cerebrovascular Disease 2005 July: 20:34-40.
3. Bassetti, Clandio L. Sleep and Stroke. Seminars in Neurology, Volume 25, Number 2 2005:19-32
4. Bowler, John V., Hachinski, Vlandimir. Vascular Dementia Clinical Summary. Medlinks Neurology. 6/1/06: 1-35.
5. Chen, Yan, Guo, Jeff J. Meta-Analysis of Antidepressant Treatment for Patients with Post-Stroke Depression (Letter to Editor) (Stroke 2006; 37:1365-1366).
6. De Groot, Marleen H. et al. Fatigue Associated with Stroke and Other Neurologic Conditions: Implication for Stroke Rehabilitation. Arch Physical Medical Rehabilitation 2003; 84:1714-1720.
7. Dumoulin, Chantale et al. Urinary Incontinence After Stroke: Does Rehabilitation Make A Difference?…….Top Stroke Rehabilitation 2002; 12(3):66-76.
8. Feleppa, Michele et al. Early Post-Stroke Seizures Clinical and Experimental Hypertension, 28: 265-270, 2006.
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Selected References (cont.)
9. Ferro, Jose M. and Pinto, Francisco Post Stroke Epilepsy……Drugs Aging 2004; 21(10):639-653.
10. Frese, A et al. Pharmacologic Treatment of Central Post-Stroke Pain Clinical Joint Pain. Volume 22, Number 3, March/April 2006.
11. Kappelle, L,J and Van Derworp, H.B. Treatment or Prevention of Complications of Acute Ischemic Stroke Current Neurology and Science Reports 2004, 4:36-41.
12. Kelly, James et al. Pulmonary Embolism and Pneumonia May Be Cofounded after Acute Stroke and May Co-Exist Age and Ageing 2002; 31:235-239.
13. Leys, Didier et al. Post-Stroke Dementia Lancet Neurology 2005; 4:752-759.
14. Moroz, Alex et al. Stroke and Neurodegenerative Disorders .2. Stroke: Comorbidities and Complications Arch Physical Medical Rehabilitation 2004;85(3 Supply 1):511-4.
15. Poole, Kenneth E.S. et al. Falls Fractures and Osteoporosis After Stroke…. (Stroke, 2002; 33:1432-1436).
16. Williams, Linda S. Depression and Stroke: Cause or Consequences? Seminars in Neurology, Volume 25, Number 4, 2005:396-409.