1. CVA, Vascular and Other Neurological Problems
Paul Logan, CRNP
N440

2. Aneurysms Weakening arterial wall causes ballooning effect.
Approximately 10% to 30% die from initial bleeding before reaching the hospital.
Additional 50% die within 1 month.
Overall mortality is as high as 65%.

3. Etiology Congenital Degenerative Acquired
Marfan’s syndrome, polycystic disease, SLE
Acquired
Traumatic brain injury
Sepsis
Cigarette smoking
Hypertension

4. Epidemiology Prevalence of 1% to 6% adults
30,000 new cases of aneurysm rupture/SAH per year
Incidence of 8 to 10 cases per 100,000 persons
Annual risk 1.34% per year
Incidence peaks between 55 and 60 years
Women > men
Seasonal increase in spring and fall

5. Common Aneurysm Sites in Circle of Willis

6. Clinical Manifestations
Silent unless ruptures
Headache
“Worst headache of my life”
Lethargy
Nausea and vomiting
Neck pain (meningeal irritation)
“Noise in the head”
Optic, oculomotor, or trigeminal CN dysfunction

7. Diagnosis History and physical examination CT scan Lumbar puncture
Cerebral angiogram
CTA
MRA
DSA

8. Management Prevent rebleeding: “aneurysm precautions”
Quiet environment, bowel regimen, limiting visitors
Antihypertensive medications
Treat hyponatremia.
Stool softeners
Pain management
Antipyretics and cooling blanket for fevers
Manage increased ICP.

9. Surgical Management and Interventional
Usually within 24 to 48 hours
Clipping
Wrapping
Coiling
Interventional therapy
Placement coils into aneurysm

10. Vasospasm Complication of SAH Occurs 3 to 12 days after SAH
Peaks 7 to 10 days
Causes cerebral ischemia
Diagnosed TCD
Treatment:
“Triple H” therapy—induced hypertension, hypervolemia, and hemodilution
Nimodipine
Balloon angioplasty/intra-arterial vasodilators

11. Other Complications of SAH
Hydrocephalus
Seizures
Rebleeding
Hyponatremia
Cerebral edema

12. Arteriovenous Malformations (AVMs)
Arterial blood flows directly into venous system.
“Tangle” of vessels
Well-defined nidus
Do not involve brain parenchyma
May contain an aneurysm
Congenital and may enlarge with age
About 90% located in the cerebrum

13. AVMs: Pathophysiology
Most likely arise at time of capillary development of fetus brain
Failure to develop adequate capillary system
4 to 8 weeks of embryo development
Less resistance due to direct shunting of blood from arterial to venous circulation
AVM receives significant blood flow.
AVM and draining vein enlarge.

14. Clinical Manifestations
Hemorrhage (intracerebral, SAH, subdural)
38% to 70% of patients
Seizures
15% to 40% of patients
Other signs include
Headache, increased ICP, neurological deficits
5% to 7% of patients

15. Diagnosis CT and MRI Angiogram MRA TCD SPECT and PET scans fMRI
Identify eloquent areas of brain

16. Management Endovascular embolization of feeding arteries
Treat small AVMs
Used as adjunct to surgery and radiosurgery
Stereotactic radiosurgery
Gamma knife
May be staged procedures
Surgery
Brain mapping

17. Neurosurgical Approaches
Stereotactic biopsy
Craniotomy
Transsphenoidal surgeries
Transnasal surgeries
Neuroendoscopy

18. Stroke
Neurological deficit that has a sudden onset, results in permanent damage to the brain
Called “brain attack”
Ischemic strokes
Embolic
Thrombotic
Hemorrhagic strokes
Intracerebral
SAH

19. Stroke Epidemiology
Approximately 780,000 new or recurrent stroke each year
Mortality rate 35%
Average age is 70 years.
Women > incidence than men
Risk factors
Prevention

20. Pathophysiology Zone of ischemia (reversible)
Zone of infarction (irreversible)
Cerebral edema
Potential herniation

21. Clinical Manifestations
Weakness
Numbness
Upper motor neuron findings
Visual changes
Dysarthria
Dysphagia
Aphasia—expressive or receptive

22. Diagnosis Rapid diagnosis essential History and physical assessment
3 to 4.5 hours to initiate tPA
History and physical assessment
NIH stroke scale
Differential diagnosis
CT scan
MRI/DWI/PWI
Cerebral angiography

23. Clinical Management: Ischemic Strokes
IV t-PA
3 to 4.5 hours
IV or intra-arterial
MERCI retriever (interventional therapy)
Up to 8 hours
Anticoagulation therapy
BP management
Treat increased ICP

24. Surgical Management
Carotid endarterectomy
Carotid Stenting

25. Management: Hemorrhagic Strokes
Intracerebral hemorrhage caused by hypertension, coagulopathies, vasculitis, sympathomimetic drugs
Diagnosis: CT scan
Management includes
Aggressive BP control
Manage increasing ICP

26. Seizures Episode of abnormal and excessive discharge of neurons
Epilepsy condition spontaneous and recurrent seizures
Status epilepticus is continued or repetitive activity.
Psychogenic nonepileptic seizures
Specific symptoms based upon location of discharge
Most common site temporal lobe

27. Etiology Idiopathic Vascular disease Alcohol Cerebral tumors or trauma
Metabolic disturbances/anoxia injury
Degenerative diseases
Developmental
Cerebrovascular disease

28. Variables that Lower Seizure Threshold
Fatigue and sleep deprivation
Emotional and physical stress
Menstruation cycle/pregnancy/menopause
Alcohol and drug abuse
Certain medications
Fever

30. Diagnosis History and physical examination Description of seizure
Family history
CT/MRI
EEG
PET/SPECT scans
fMRI
Epilepsy monitoring unit

31. Intractable Seizures in Children…
What can be offered to children with intractable seizures?
Strict ketogenic diet
Surgery—Hemispherectomy can be performed prior to age 6, or so.
Who revitalized the hemispherectomy at Johns Hopkins in the 1980s?

33. Ben Carson, MD

34. Management
Antiepileptic agents—Keppra (levitracetam) has revolutionized medical management
Localize seizure focus
Surgery
Temporal lobectomy
Hemispherectomy
Corpus callosectomy
Vagal nerve stimulator
Deep brain stimulator