Transcript Neurological and Medical Complication of Stroke Harvey A. Drapkin, D.O. F.A.C.N.

Neurological and Medical
Complication of Stroke
Harvey A. Drapkin, D.O.
F.A.C.N.
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.
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.
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.
Slide of Cerebral Infarct with
Edema
Slide of Cerebral Infarct with
Edema
Treatment of Increased
Intracranial Pressure
• Osmotic Agents
• Hyperventilation
• External Ventricular Drainage
Hypoxia, Hypercapnia and Hyperthermia
must be avoided.
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.
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.
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.
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.
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.
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%.
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
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 multidisciplinary stroke unit.
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.
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
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.
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.
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
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
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!
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 reexperience?
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
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
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 NonPharmacologic
Cognitive Syndrome of PostStroke Dementia
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•
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•
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
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
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 – DEAFFFacil./Inhib. Imbalance
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
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.
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
Other Complications of Stroke
• Falls, Fractures, Osteoporosis
Prophylactic I.V. Bisphosphonates??
• Voiding and Sexual Dysfunction
Medical – Urological – Rehabilitation –
Nursing Team Approach
Secondary Stroke Prevention
• 200,000 of Total Strokes
• Profound effect on Morbidity-Mortality
• ABCDE Treatment options
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–
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A – Anti-platelet, Anticoag., Art. Revascularization
B – Blood pressure control
C - Cholesterol, Cig. Cessation
D – Diet
E – Exercise
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.
Selected References:
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Annoni, Jean-Marie et al. Emotional Disturbances after Stroke, Clinical and Experimental
Hypertension 28:243-249, 2006.
Appelros P. et al. Lacunar Infarcts, Functional and Cognitive Outcomes……Cerebrovascular
Disease 2005 July: 20:34-40.
Bassetti, Clandio L. Sleep and Stroke. Seminars in Neurology, Volume 25, Number 2 2005:19-32
Bowler, John V., Hachinski, Vlandimir. Vascular Dementia Clinical Summary. Medlinks
Neurology. 6/1/06: 1-35.
Chen, Yan, Guo, Jeff J. Meta-Analysis of Antidepressant Treatment for Patients with Post-Stroke
Depression (Letter to Editor) (Stroke 2006; 37:1365-1366).
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.
Dumoulin, Chantale et al. Urinary Incontinence After Stroke: Does Rehabilitation Make A
Difference?…….Top Stroke Rehabilitation 2002; 12(3):66-76.
Feleppa, Michele et al. Early Post-Stroke Seizures Clinical and Experimental Hypertension, 28:
265-270, 2006.
Selected References (cont.)
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Ferro, Jose M. and Pinto, Francisco Post Stroke Epilepsy……Drugs Aging 2004; 21(10):639-653.
Frese, A et al. Pharmacologic Treatment of Central Post-Stroke Pain Clinical Joint Pain. Volume
22, Number 3, March/April 2006.
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.
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.
Leys, Didier et al. Post-Stroke Dementia Lancet Neurology 2005; 4:752-759.
Moroz, Alex et al. Stroke and Neurodegenerative Disorders .2. Stroke: Comorbidities and
Complications Arch Physical Medical Rehabilitation 2004;85(3 Supply 1):511-4.
Poole, Kenneth E.S. et al. Falls Fractures and Osteoporosis After Stroke…. (Stroke, 2002;
33:1432-1436).
Williams, Linda S. Depression and Stroke: Cause or Consequences? Seminars in Neurology,
Volume 25, Number 4, 2005:396-409.