Exam 3 Neuro Disease Flashcards
Cerebral blood flow (CBF) is modulated by:
- cerebral metabolic rate
- cerebral perfusion pressure (CPP) * MAP-ICP
- arterial blood carbon dioxide (Paco2)
- arterial blood oxygen (Pao2)
- various drugs and intracranial pathologies
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- With autoregulation, CBF is approx ____ brain tissue per minute.
- which = ____ml/min
- and is ____% of COP
50 mL/100g
750 ml/min
15%
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- The intracranial & spinal vault contains ____, ____, and ____.
- The vault is enclosed by the ____ and ____.
- neural tissue (brain + spinal cord), blood, and CSF
- dura mater and bone
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Under normal conditions, brain tissue, intracranial CSF, and intracranial blood have a combined volume of
1200-1500mL
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at a volume of 1200-1500ml, what is a normal ICP?
5-15 mmhg
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any increase in one component of intracranial volume must be offset by a decrease in another component to prevent an elevated ICP
monro-kellie hypothesis
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During normal physiologic conditions, changes in one component are well compensated for by changes in other components, but eventually a point is reached where even a small change in intracranial contents results in a ____.
large change in ICP
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Since ICP is one of the determinants of CPP, homeostatic mechanisms canincrease MAP to support CPP despite increases in ICP, but eventually these compensatory mechanisms can fail, resulting in ____
cerebral ischemia
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The intracranial vault is considered ____
compartmentalized
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Meningeal barriers separate the brain contents and include ____ and ____.
- falx cerebri
- tentorium cerbelli
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what is the falx cerebri:
a reflection of dura that separates the two cerebral hemispheres
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what is the tentorium cerebelli:
a reflection of durathat lies rostral to the cerebellum and marks the border btw the supratentorial and infratentorial spaces
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____ in the contents of one region may cause regional increases in ICP, and in extreme instances, the contents can herniate into a different compartment
Increases
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Herniation syndromes are categorized based on the ____
region of brain affected
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types of herniation
subfalcine
transtentorial
uncal
cerebellar tonsils
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what is SubfalcineHerniation?
Herniation of hemispheric contents under the falx cerebri; typically, compressing branches of theanterior cerebral artery, creating a midline shift
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what is transtentorialHerniation?
- Herniation of the supratentorial contents past the tentorium cerebelli, causing brainstemcompression in a rostral to caudal direction.
- This leads to AMS, defects in gaze and ocular reflexes, hemodynamic andrespiratory compromise, and death
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what is Uncal Herniation?
- a subtype of transtentorial herniation, where the uncus (medial portion of temporal lobe) herniatesoverthe tentorium cerebelli.
- This results in ipsilateral oculomotor nerve dysfunction
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s/s of uncal herniation
- pupillary dilatation
- ptosis
- lateral deviation of the affected eye
- brainstem compression
- death
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when does cerebellar tonsils herniation occur?
Herniation of the cerebellar tonsils can occur due to elevated infratentorial pressure, causing the cerebellarstructures to herniate through the foramen magnum
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s/s of cerebellar tonsils herniation
medullary dysfunction, cardiorespiratory instability and subsequently death
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what type of herniation is 1, 2, 3, and 4?
- Subfalcine
- Transtentorial
- Cerebellar contents through foramen magnum
- Traumatic event causing herniation out of cranial cavity
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what can cause increased ICP?
- tumors
- intracranial hematomas
- blood in CSF
- infections
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how can tumors increase ICP?
1) directly because of their size
2) indirectly by causing edema in surrounding brain tissue
3) by obstructing CSF flow, as seen with tumors involving the third ventricle
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how can intracranial hematomas increase ICP?
Intracranial hematomas cause increased ICPsimilar to mass lesions
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how can blood in the CSF increase ICP?
Blood in the CSF, as is seen in subarachnoid hemorrhage, may lead to obstruction of CSF reabsorption, and granulations can further exacerbate increased ICP
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how can infections increase ICP?
Infections s/a meningitis or encephalitis, can lead to edema or obstruction of CSF reabsorption
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how do you decrease ICP?
- elevation of the head
- hyperventilation
- csf drainage
- hyperosmotic drugs
- diuretics
- corticosteroids
- cerebral vasocnstricting anesthetics
- surgical decompression
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how can elevation of the head decrease ICP?
encourages jugular venous outflow
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how canhyperventiltion decrease ICP?
lowers PaC02
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how can you drain CSF to decrease ICP?
external ventricular drain (EVD)
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how canhyperosmotic drugs decrease ICP?
increase osmolarity, drawing fluid across BBB
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how can diuretics decrease ICP?
induce systemic hypovolemia
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how can corticosteroids decrease ICP?
decrease swelling and enhance the integrity of the BBB
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how can cerebral vasoconstricting anesthetics decrease ICP? what medication is an example of this?
- decrease CMR02 and CBF
- propofol
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what to know for neurological assessment
- Know the basic pathophysiology for neurological disorders
- Look at patients’ history, symptoms, and baseline neuro-deficits
- Review imaging and available neurological testing results
- Review the patients’ current drugs and treatments
- Evaluate the potential risks/benefits of various anesthetic options to determine the most appropriate plan of care
- Implement pre-op measures that may help optimize the patients’ condition prior to anesthesia
- Provide clear pre-op documentation of the factors above, and have a rational for chosen anesthetic plan
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what are examples of genetic neurological disorders
Multiple Sclerosis
Myasthenia Gravis
Lambert Eaton Syndrome
Myasthenia Syndrome
Muscular Dystrophies
Myotonic Dystrophies
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- This is a progressive, autoimmune demyelination of central nerve fibers.
- There is an onset at age 20-40.
- Risk factors include: female, 1st deg relative, EBV, other AI disorders, smoking
- Characterized by periods of exacerbations & remissions
- Triggers: stress, elevated temps, postpartum period
- Sx: motor weakness, sensory disorders, visual impairment, autonomic instability. Sx vary b/o site of demyelination
- Tx: No cure
multiple sclerosis “MS”
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although MS has no cure it can be managed with:
- corticosteroids
- immune modulators
- targeted antibodies
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what preanesthetic considerations should be thought of with a patient with MS?
- Assess existing deficits
- If respiratory compromise, consider pulmonary function tests
- Labs: CBC, BMP, +/-LFT
- LFT if on Dantrolene & Azathioprine (bone marrow suppression, liver function impairment)
- Close attn to glucose and electrolytes as steroids may impact levels
- Consider giving pre-op steroids in anyone with long-term steroid use
- LT steroids cause adrenal suppression, so a stress-dose of steroids may be necessary for surgery
- Temperature management is critical
- Any increase in body temp can precipitate an exacerbation of MS sx
- GA, RA & PNB’s are acceptable options
- Avoid Succinylcholine as it may induce hyperkalemia
- Upregulated N-ach receptors
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What is this disease?
* Autoimmune; Antibodies generated against N-Ach-R’s at skeletal motor endplate
* Effects skeletal muscle, not smooth or cardiac muscle
* Muscle weakness, exacerbated w/exercise
* Cranial nerves partially susceptible
* Ocular sx common-diplopia, ptosis
* Bulbar involvement → laryngeal/pharyngeal weakness→ respiratory insufficiency, aspiration rx
* Thymic-hyperplasia is common (10%)
* 90% pts improve after Thymectomy
Myasthena Gravie “MG”
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For Myasthenia Gravie “MG”
* S/S exacerbated by:
* Tx:
- S/S exacerbated by: pain, insomnia, infection, surgery
- Tx: Ach-E inhibitors (Pyridostigmine), immunosuppressive agents, steroids, plasmapheresis, IVIG
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MG preanesthetic considerations include:
- If respiratory compromise, consider pulmonary function tests
- Optimize respiratory function
- Reduce paralytic dosage to avoid prolonged muscle weakness
- Caution with opioids to avoid respiratory compromise
- Ach-E inhibitors may prolong Succs and Ester LA’s
- Labs: CBC, BMP, +/-LFT (LFT if on Azathioprine)
- Close attn to glucose and electrolytes as steroids may impact levels
- Consider pre-op steroids in anyone with long-term steroid use
- Counsel patients on the increased risk of needing post-op resp support/ventilation until fully recovered from anesthesia
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what is this disease:
* Disorder causing the development of autoantibodiesagainst VG Calcium chnls
* Reduce Ca++ influx into the presynaptic Ca++ channels→↓Ach release @ the NMJ
* Sx similar to MG
* >60% cases areassoc w/ small cell lung carcinoma
eaton-lambert syndrome
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for eaton-lambert syndrome:
* s/s
* tx:
- Sx: progressive limb-girdle weakness, dysautonomia, oculobulbar palsy
- Tx: Selective K+ chnl blocker “3-4 diaminopyridine”, Ach-E inhibitors, immunologics (Azathioprine), steroids, plasmapheresis, IVIG
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ELS pre-anesthetic considerations include:
- Assess existing deficits
- If respiratory compromise, consider pulmonary function tests
- VERY sensitive to ND-NMB & D-NMB
- Significantly more sensitive to ND-NMB than MG patients
- Optimize respiratory function
- Extreme caution on paralytic and opioid dosing
- Counsel on risks for needing post-op resp support until fully recovered from anesthesia
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what is this disease?
* Hereditary disorder of muscle fiber degeneration c/b breakdown of the dystrophin-glycoprotein complex, leads to myonecrosis, fibrosis, and skeletal muscle mbrn permeability.
muscular dystrophy
6 typer of MD
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what is the most common and severe form of muscular dystrophy?
- Ducheen MD
- Occurs only in boys, onset 2-5y. Wheelchair bound by age 8-10. Avg lifespan ̴20-25y d/t cardiopulmonary complications
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for muscular dystrophy:
* S/S:
- progressive muscle wasting without motor/ sensoryabnormalities
- kyphoscoliosis
- long bone fragility
- respiratory weakness
- frequent pneumonia
- EKG changes
- Elevated serum creatine kinase c/b muscle wasting
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MD preanesthetic considerations
- CBC, BMP, PFTs, consider CK
- Pre-op EKG, echocardiogram. Evaluate for cardiomyopathy
- Caution with ND-NMB’s, careful monitoring throughout
- “Hypermetabolic Syndrome” similar to MH seen with Succs & volatile anesthetics
- Hypermetabolic syndrome can lead to: rhabdomyolysis, hyperkalemia, Vfib, cardiac arrest
- Avoid Succs & VA as they exacerbate instability of muscle membrane
- Consider low dose rocuronium and TIVA for GA
- Have MH cart with Dantrolene available
- RA preferred over GA to avoid triggers and cardiopulmonary complications
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what are the myotonic dystrophies mentioned in class?
- myotonia
- myotonic dytrophy
- myotonia congenita
- central core disease
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what is myotonia?
- prolonged contraction after muscle stimulation
- seen in several muscle disorders
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what is myotonic dystrophy? what is its s/s?
- most common myotonia. Onset 20-30’s
- Sx: muscle wasting in face, masseter, hand, pre-tibial muscles
- may also affect pharyngeal, laryngeal, diaphragmatic muscles
- cardiac conduction may be affected; 20% have MVP
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what is myotonia congenita?
- Milder form, involving theskeletal muscles
- smooth & cardiac muscles are spared
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what is central core disease? s/s? tx?
- Rare. Core muscle cells lack mitochondrial enzymes
- Sx:Proximal muscle weakness & scoliosis
- Myotonias are triggered by stress & cold temps
- Tx: No cure. Sx managed w/Quinine, Procainamide, Steroids
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pre-anesthetic considerations for myotonic dystrophies?
- Assess the extent of cardiac and pulmonary abnormalities
- Assess breath and heart sounds for abnormalities
- GI hypomotility-↑aspiration risk
- High rx of endocrine abnormalities. Look at thyroid & glucose levels
- Keep patients warm to avoid flare-ups
- Avoid Succinylcholine b/c fasciculations trigger myotonia
- Optimize preop respiratory status
- Caution with opioids to avoid post-op respiratory depression
- Pts are increased risk for post-op resp weakness
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what are the 3 major dementia syndromes?
Alzheimer’s (70%), Vascular dementia (25%), Parkinsons (5%)
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what are the triad of sx in parkinsons? what are other s/s?
- Triad:
- skeletal muscle tremor, rigidity, akinesia
- Other:
- Rhythmic “pill rolling,”
- facial rigidity,
- slurred speech,
- difficulty swallowing,
- respiratory difficulty,
- depression
- dementia
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common s/s of brain tumors
- ↑ICP
- Papilledema
- Headache
- AMS
- Mobilityimpairment
- Vomiting
- Autonomic dysfunction
- Seizures
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what are the types of strokes/CVAs?
- ischemic
- hemorrhagic
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clinical features of occluded anterior cerbral artery
contralateral leg weakness
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clinical features of occluded middle cerbral artery
- controlateral hempiparesis and hemisenory deficit face and arme > leg
- aphasia dominat hemisphere
- controlateral visual field defect
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clinical features of occluded posterior cerbral artery
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clinical features of occluded penetrating arteries
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clinical features of occluded basilar artery
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clinical features of occluded verterbral artery
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what is the hunt and hess classification for grading aneurysm prognosis?
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what is the world federation of neurologic surgeon grading system for grading aneurysm prognosis?
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what 3 things does the spetzier martin AVM grading system look at?
- Nidus size
- eloquence of adjacent brain
- pattern of venous drainage
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what are the surgical outcomes based on the spetzler martin AVM Grade:
* 1
* 2
* 3
* 4
* 5
percent of patient with no postoperative neurological deficit
* 1= 100%
* 2= 95%
* 3= 84%
* 4= 73%
* 5= 69%
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what is chiari malformation?
Congenital displacement of the cerebellum
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what are the 4 types of chiarir malformation?
- Type 1: downwarddisplacement ofcerebellum
- Type 2 (Arnold Chiari):downwarddisplacementofcerebellar vermis, often assoc w/myelomeningocele
- Type 3: Rare; occipital encephalocele w/downward cerebellar displacement
- Type 4: cerebellar hypoplasia w/o displacement of posterior fossa contents
- Not compatible with life
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what is AKA “Bourneville Disease”
and is an autosomal dominant disease causing benign hemartomas, angiofibromas, and other malformations that can occur anywhere in the body
tuberous sclerosis
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what is an autosomal dominant disease where benign tumors of the CNS, eyes, adrenals, pancreas and kidneys occur. And it may present w/ pheochromocytoma?
von hippel-lindau disease
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traumatic brain injury is categorized as ____ or ____ by using ____ to categorize the severity
- “penetrating” or “non-penetrating,” d/o breech of dura
- Severity categorized by Glasco-Coma Scale
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