Neurological Diseases Flashcards
Exam 3
CBF is modulated by what 5 things?
- cerebral metabolic rate
- cerebral perfusion pressure (CPP)
- arterial blood carbon dioxide (PaCO2)
- arterial blood oxygen (PaO2)
- various drugs and intracranial pathologies
CPP formula
CPP = MAP-ICP
With autoregulation, CBF is approx _____ brain tissue per minute; mL/min? __% of CO?
50 mL/100g
- 750ml/min
- 15% of COP
The intracranial & spinal vault contains what 3 things?
neural tissue (brain + spinal cord), blood, and CSF
The intracranial & spinal vault is enclosed by what?
the dura mater and bone
Under normal conditions, brain tissue, intracranial CSF, and intracranial blood have a combined volume of _______. At this volume, ICP is _______
1200-1500mL
5-15 mmHg
What is the Monro-Kellie hypothesis?
any increase in one component of intracranial volume must be offset by a decrease in another component to prevent an elevated ICP; eventually, compensatory mechanisms can fail, resulting in cerebral ischemia
The intracranial vault is considered ____________
compartmentalized
What are the meningeal barriers that separate the brain contents?
the falx cerebri and the tentorium cerebelli
__________ is a reflection of dura that separates the two cerebral hemispheres
the falx cerebri
____________ is a reflection of durathat lies rostral to the cerebellum and marks the border btw the supratentorial and infratentorial spaces
the tentorium cerebelli
Herniation syndromes are categorized based on what?
the region of brain affected
Herniation of hemispheric contents under the falx cerebri; typically, compressing branches of theanterior cerebral artery. What does this type of herniation lead to?
Subfalcine Herniation
- creating a midline shift
Herniation of the supratentorial contents past the tentorium cerebelli, causing brainstemcompression in a rostral to caudal direction. What does this type of herniation lead to?
Transtentorial Herniation
- This leads to AMS, defects in gaze and ocular reflexes, hemodynamic andrespiratory compromise, and death
A subtype oftranstentorial herniation, where the uncus (medial portion of temporal lobe)herniatesoverthe tentorium cerebelli. What does this type of herniation result in?
Uncal Herniation
- This results in ipsilateral oculomotor nerve dysfunction
What are the s/s of uncal herniation?
Pupillary dilatation, ptosis, and lateral deviation of the affected eye, brainstem compression and death
Herniation of the ____________ can occur due to elevated infratentorial pressure, causing the cerebellarstructures to herniate through the foramen magnum
cerebellar tonsils
What are the s/s of herniation of the cerebellar tonsils?
Sx: medullary dysfunction, cardiorespiratory instability and subsequently death
What are the 4 brain herniation examples?
- Subfalcine
- Transtentorial
- Cerebellar contents through foramen magnum
- Traumatic event causing herniation out of cranial cavity
What are the 4 causes of increased ICP?
Tumors, intracranial hematomas, blood in the CSF, and infections
What are the 3 ways that tumors can lead to increased ICP?
- directly because of their size
- indirectly by causing edema in surrounding brain tissue
- by obstructing CSF flow, as seen with tumors involving the third ventricle
What are the non-pharmacologic methods to decrease ICP?
- Elevation of the head: encourages jugular venous outflow
- Hyperventilation: lowers PaC02
- CSF drainage: external ventricular drain (EVD)
- Surgical decompression
What are the pharmacologic methods to decrease ICP?
- Hyperosmotic drugs: increase osmolarity, drawing fluid across BBB
- Diuretics: induce systemic hypovolemia
- Corticosteroids: decrease swelling and enhance the integrity of the BBB
- Cerebral vasoconstricting anesthetics (propofol): decrease CMR02 and CBF
What are the 6 genetic neurologic disorders?
- Multiple Sclerosis
- Myasthenia Gravis
- Lambert Eaton Syndrome
- Myasthenia Syndrome
- Muscular Dystrophies
- Myotonic Dystrophies
______ is a progressive, autoimmune demyelination of central nerve fibers
MS
What is the onset age of MS? Risk factors?
- Onset age 20-40
- Rx factors: Female, 1st deg relative, EBV, other AI disorders, smoking
MS is characterized by what?
Characterized by periods of exacerbations & remissions
What are the triggers for MS?
Triggers: stress, elevated temps, postpartum period
What are the s/s of MS?
Sx: motor weakness, sensory disorders, visual impairment, autonomic instability. Sx vary b/o site of demyelination
What is the tx for MS?
No cure - managed with corticosteroids, immune modulators, targeted antibodies
What labs are considered before anesthesia in MS and MG?
CBC, BMP, +/-LFT
- LFT if on Dantrolene & Azathioprine(bone marrow suppression, liver function impairment)
Why should sux be avoided in MS patients?
induces hyperkalemia - upregulated nACh-R
__________ is an autoimmune disorder in which antibodies are generated against nAC-R at the skeletal motor endplate
MG
Which muscles are effected in MG?
Effects skeletal muscle, not smooth or cardiac muscle
What are the s/s of MG with cranial nerve involvement?
- Ocular sx common-diplopia, ptosis
- Bulbar involvement → laryngeal/pharyngeal weakness→ respiratory insufficiency, aspiration rx
What are the general s/s of MG?
Muscle weakness, exacerbated w/exercise, pain, insomnia, infection, and sx
How common is thymic-hyperplasia in MG? What is the tx?
10% - thymectomy
What is the tx for MG?
Tx: Ach-E inhibitors (Pyridostigmine), immunosuppressive agents, steroids, plasmapheresis, IVIG
Which anesthesia meds have altered responses in pts with MG?
- 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
_________ is a disorder resulting in the development of auto-antibodiesagainst VG Calcium channels
Eaton-Lambert Syndrome
- Reduce Ca++ influx into the presynaptic Ca++ channels→↓Ach release @ the NMJ
Eaton-Lambert Syndrome is associated with what?
small cell lung carcinoma
What are the s/s of Eaton-Lambert Syndrome?
Similar to MG - progressive limb-girdle weakness, dysautonomia, oculobulbar palsy
What is the tx of Eaton-Lambert Syndrome?
Selective K+ chnl blocker “3-4 diaminopyridine”, Ach-E inhibitors, immunologics (Azathioprine), steroids, plasmapheresis, IVIG
Which meds are ELS pts sensitive to?
- VERY sensitive to ND-NMB & D-NMB
- Significantly more sensitive to ND-NMB than MG patients
- Extreme caution on paralytic and opioid dosing
______ is a hereditary disorder of muscle fiber degeneration c/b breakdown of the dystrophin-glycoprotein complex
Muscular Dystrophy
What is the most common type of MD? How many types are there?
Duchenne MD = most common & severe form
- 6 types
Which genetic neurologic disorder is associated with MH?
MD - avoid sux, VA, ND-NMBDs
- hypermetabolic syndrome
What are the s/s of MD?
Sx: progressive muscle wasting w/o motor/sensoryabnormalities, kyphoscoliosis, long bone fragility, respiratory weakness, frequent pneumonia, EKG changes
- Elevated serum creatine kinase c/b muscle wasting
What is the onset, WCB age, and average lifespan of Duchenne MD pts?
Occurs only in boys, onset 2-5y. Wheelchair-bound by age 8-10. Avg lifespan ̴20-25y d/t cardiopulmonary complications
What labs should be obtained prior to anesthesia in patients with MD?
CBC, BMP, PFTs, consider CK
What kind of anesthesia can be given to pts with MD?
- Consider low dose rocuronium and TIVA for GA
- RA preferred over GA to avoid triggers and cardiopulmonary complications
ACh-E inhibitors prolong what drugs?
sux and ester LA’s
______ is prolonged contraction after muscle stimulation
myotonia
What is the most common myotonia? Onset?
Myotonic Dystrophy
- Onset 20-30’s
What are the s/s of Myotonic Dystrophy?
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
_______ is a milder type of myotonia involving the skeletal muscles (smooth & cardiac muscles are spared)
Myotonia Congenita
________ is a rare form of myotonia in which core muscle cells lack mitochondrial enzymes
Central Core disease
What are the s/s of Central Core disease?
- Proximal muscle weakness & scoliosis
- Myotonias are triggered by stress & cold temps
What is the tx for central core disease?
Tx: No cure. Sx managed w/Quinine, Procainamide, Steroids
What are patients with myotonia disorders at higher risk for under anesthesia?
- GI hypomotility-↑aspiration risk
- High rx of endocrine abnormalities (check thyroid & glucose levels)
- Pts are at increased risk for post-op resp weakness
What meds should be avoided or given with caution in pts with myotonia disorders?
- Avoid Succinylcholine b/c fasciculations trigger myotonia
- Caution with opioids to avoid post-op respiratory depression
What are the 3 major dementia syndromes?
Alzheimer’s (70%), vascular dementia (25%), and Parkinson’s (5%)
Patients with dementia syndromes are at increased risk for what under anesthesia? What type of anesthesia is ideal?
- aspiration
- ↑risk for post-op delirium (consider TIVA)
- RA preferred to ↓opioid requirements
__________ is the degeneration of dopaminergic fibers of basal ganglia
Parkinsons Disease
What is the cause and pathophysiology of Parkinsons Disease?
- Unknown cause; Advanced age is biggest risk factor
- Dopamine regulates (inhibits excess stimulation) the extrapyramidal motor system, which is stimulated by Ach
- In Parkinsons, these motor neurons are over stimulated
What is the Parkinsons triad? What are the other s/s?
Triad of sx: skeletal muscle tremor, rigidity, akinesia
- Rhythmic “pill rolling,” facial rigidity, slurred speech, difficulty swallowing, respiratory difficulty, depression & dementia
What is the tx for Parkinsons?
Tx: Levodopa (crosses BBB), anticholinergics, MAOIs (inhibit dopamine degradation), Deep brain stimulator
What meds should be avoided in patients with Parkinsons?
- PO Levodopa must be continued to avoid unstable extreme extrapyramidal effects s/a chest wall rigidity
- Avoid Reglan, Phenothiazines, Butyrophenones
- Avoid Demerol if on MAOI
What consideration is necessary in Parkinson’s pts with deep brain stimulators?
- Deep brain stimulators may need to be disabled to avoid interaction w/cautery
- If cautery used, bipolar recommended as it reduces the scattering of electro-currant
What are common s/s of brain tumors? (8)
- ↑ICP
- Papilledema
- Headache
- AMS
- Mobilityimpairment
- Vomiting
- Autonomic dysfunction
- Seizures
_________ are the most common CNS glial cells
Astrocytes
What are the 4 types of Astrocytomas?
Gliomas, pilocytic astrocytomas, anaplastic astrocytomas, glioblastoma multiforme
Name the Astrocytoma type: Primary tumors, least aggressive astrocytomas often found in young adults with new-onset seizures
Gliomas
Name the Astrocytoma type: mostly benign tumors in children and young adults that have good outcomes with resection
Pilocyctic astrocytomas
Name the Astrocytoma type: poorly differetiated, usually evolves into Glioblastoma Multiforme
Anaplastic astrocytomas
Name the Astrocytoma type: carry a high mortality - life expectancy within weeks even w/ tx (requires sx debulking and chemo)
Glioblastoma Multiforme
Name the brain tumor type: Arise from dura or arachnoid tissue; usually benign - good prognosis w/surgical resection
Meningiomas
Name the brain tumor type: Noncancerous, varying subtypes; - Transsphenoidalor open craniotomy for removal is usually curative
Pituitary Adenomas
Name the brain tumor type: -Usually benign schwannomas involving the vestibular component of CN VIII within the auditory canal (Good prognosis w/resection +/- radiation)
Acoustic Neuromas
Name the brain tumor type: can vary widely in origin &symptoms; outcomes are generally less favorable
Metastatic carcinomas
Why are pts with brain tumors usually on steroids?
to minimize cerebral edema
________ are commonly used in pts w/ supratentorial lesions, closer to motor cortex
Anticonvulsants
________ can be used to reduce intracranial volume & pressure in pts w/ brain tumors
Mannitol
_____ is the leading cause of death and disability, worldwide
stroke
2 stroke types
- ischemia (88% of cases)
- hemorrhage (12% of cases)
Blood is supplied to the brain from:
internal carotid arteries and vertebral arteries
Clinical features of an occluded anterior cerebral artery
contralateral leg weakness
Clinical features of an occluded middle cerebral artery
contralateral hemiparesis and hemisensory deficit (face and arm more than leg), aphasia (dominant hemisphere), and contralateral visual field defect
Clinical features of an occluded posterior cerebral artery
contralateral visual field defect and contralateral hemiparesis
Clinical features of an occluded penetrating artery
contralateral hemiparesis and contralateral hemisensory deficits
Clinical features of an occluded basilar artery
oculomotor deficits and/or ataxia with crossed sensory and motor deficits
Clinical features of an occluded vertebral artery
lower cranial nerve deficits and/or ataxia with crossed sensory deficits
____________ occlusion of a vessel that supplies a region of brain resulting in cellular ischemia
ischemic stroke
______________ a sudden focal vascular neurologic deficit that resolves within 24 hrs
Transient ischemic attack
____ of pts who experience a TIAwill subsequently suffer a stroke
1/3
Thrombolytic intervention should occur within ______ of an ischemic stroke
90 min
How can youdistinguish an ischemia strokefrom an intracerebral hemorrhage?
non-contrast CT
What are the 5 classifications of ischemic stroke causes according to the TOAST?
- Large artery atherosclerosis (e.g., carotid stenosis)
- Small vessel occlusion (e.g., lacunar stroke)
- Cardioaortic embolic (e.g., emboli from atrial fibrillation)
- Other etiology (e.g., stroke due to hypercoagulable states or vasculopathies)
- Undetermined etiology
What is the tx for an ischemic CVA?
PO aspirin, tissue plasminogen activator (TPA), and revascularization
Patients w/ ischemic stroke frequently have __ risk factors
CV - HTN, DM, CAD, Afib, andvalvular disease, that could impact vasoactive drug choices and hemodynamic goal
________ is bleeding inside the cranial vault that impairs perfusion of the brain
Hemorrhagic stroke
Hemorrhagic stroke is __ more likely to cause death than ischemic stroke
4x
The 2 most reliable predictors of outcome in a hemorrhagic stroke are:
estimated blood volume & change in LOC
What are the 5 subtypes of hemorrhagic strokes?
Based on location of blood:
- Bloodwithin the brain: intraparenchymal hemorrhage
- Blood in the epidural space: epidural hematoma
- Blood in the subdural space: subdural hematoma
- Blood in subarachnoid space: subarachnoid hemorrhage
- Blood located in the ventricular system: intraventricular hemorrhage (usually occurs in conjunction with other types of hemorrhagic stroke)
What is the tx of a hemorrhagic stroke?
Conservative tx: reduction of ICP,blood pressure control, seizure precautions, and vigilant monitoring
- Surgical treatment involves evacuation of the hematoma
What are the 3 types of neurologic vascular disorders?
- Cerebral vascular disease
- Aneurysms
- Arteriovenous Malformations
If a pt w/ cerebrovascular disease is on a new anticoagulant for thrombus, how long must they wait for elective sx?
3 months
How often are cerebral aneurysms diagnosed before rupture?
- Majority aneurysms not diagnosed before rupture
- Only1/3 aneurysm pts have sx before rupture
What are the s/s of cerebral aneurysms?
Headache, photophobia, confusion, hemiparesis, coma
What are the risk factors of cerebral aneurysms?
HTN, smoking, female, oral contraceptives, cocaine use
How are cerebral aneurysms diagnosed?
CT/angio, MRI, Lumbar puncture w/CSF analysis if rupture suspected
Intervention for cerebral aneurysms should be performed within ___ of rupture for best outcomes. What is the sx tx?
72 hours
- Surgical tx: coiling, stenting, trapping/bypass (very large aneurysms)
How long after SAH are patients at risk for vasospasm?
3-15 days post SAH
What is the patho of Post-SAH Vasospasms?
Free hgb triggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin 1, leading to vasoconstriction
What is the triple H therapy for post-SAH vasospasm?
Hypertension, Hypervolemia, Hemodilution
- To avoid complications of hypervolemia, HTN is the initial main treatment
- Interventional treatments s/a balloon dilation and direct injection of vasodilators relieve the spasm
Hunt and Hess classification for aneurysms
Scores 0-5 - 5 has 40-50% mortality
1. unruptured
2. ruptured w/ min HA and no neuro deficits
3. mod-severe HA, no deficit other than cranial nerve palsy
4. drowsiness, confusion, or mild focal motor deficit
5. stupor, sig hemiparesis, early decerebration
6. deep coma, decerebrate rigidity
Glasgow coma scale score for aneurysms
0-5
0 - intact, unruptured aneurysm
1 - score 15, no major focal deficit
2 - score 13-14, no major focal deficit
3 - score 13-14, with major focal deficit
4 - score 7-12, may have major focal deficit
5 - score 2-6, may have major focal deficit
________ is an arterial to venous connection w/o intervening capillaries that creates an area of high flow, low resistance shunting; believed to be congenital
Arteriovenous Malformations “AVM”
The majority of AVMs are ______
supratentorial
What are the s/s of AVMs? Dx?
Sx: range from mass-effects to hemorrhage
Dx: Angiogram, MRI
Spetzler-Martin AVM grading system
1-5: dep on nidus size, eloquence of adjacent pain, and pattern of venous drainage
1 = 100% pts w/ no post-op neuro deficit
5 = 69% pts w/ no post-op neuro deficit
What are the 4 congenital brain diseases?
- Chiari Malformations
- Tuberous Sclerosis
- Von Hippel-Lindau Dz
- Neurofibromatosis
________ is a congenital brain abnormality with displacement of the cerebellum
Chiari Malformation
What are the 4 types of Chiari 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
What are the s/s of Chiari Malformation? Tx?
Sx: headache, extending to shoulders/arms,visual disturbances, ataxia
Tx: Surgical decompression
What is the other name for Tuberous Sclerosis?
Bourneville Disease
_____________ is an autosomal dominant disease, causing benign hemartomas, angiofibromas, and other malformations that can occur anywhere in the body
Tuberous Sclerosis
What lesions of the brain are included in Tuberous Sclerosis? What other areas are often involved?
cortical tumors & giant-cell astrocytomas
- Often involves co-existing tumors of face,oropharnyx, heart, lungs, liver &kidneys
How does Tuberous Sclerosis present?
mental retardation and seizure disorders
___________ is a genetic disease process involving formations of benign tumors of the CNS, eyes, adrenals, pancreas and kidneys
Von Hippel-Lindau Disease
Von Hippel-Lindau Disease may present with ________. Anesthetic consideration?
pheochromocytoma - exaggerated HTN
What are the 3 types of neurofibromatosis?
Type 1 (most common)
Type 2
Schwannomatosis (rare)
What are the anesthetic considerations for pts w/ neurofibromatosis
- increased ICP, airway issues, scoliosis, possibility of pheochromocytoma
- Avoid NA d/t high likelihood of spinal tumors
_______ is the excessive CSF accumulation, causing ↑ICP, leading to ventricular dilatation; due to an imbalance between CSF production and absorption
Hydrocephalus
What is the tx for Hydrocephalus?
- diuretics (furosemide & acetazolamide decrease CSF production)
- Serial lumbar punctures as a temporizing measure
- The majority of cases require surgical treatment VP shunt or ETV
Hydrocephalus can be caused by
congenital or acquired d/t meningitis, tumors,head injury, or stroke
A VP shunt is a drain placed in the ______ of the brain and empties into the ________
ventricle, peritoneum (Ventriculoperitoneal)
ETV: catheter placed into the __________ that drains into the ________, __________, or more rarely the _________
lateral ventricle
peritoneal space, right atrium, or pleural space
(endoscopic third ventriculostomy)
Shunt malfunction occurs most frequently in the ________ of placement (high failure rate)
first year
How are TBIs categorized?
“penetrating” or “non-penetrating,” d/o breech of dura
- Severity categorized by Glasco-Coma Scale
Differentiate between primary and secondary injuries in TBIs
- Primary injury: occurs at time of insult
- Secondary injuries: neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, and neurogenic shock
When is intubation required in severe TBI?
GCS <9, AW trauma, resp distress
What are the pre-anesthesia considerations for TBIs?
Do not delay emergent surgery
- C-spine stabilization, adequate IV access, CVC, Aline
- uncrossmatched blood if no time for T & C
- Refrain from NGT/OGT –potential for basal skull fx
- Intra-op ISTAT labs, Pressors, Bicarb, Calcium, & Blood products
Glasgow coma score components
eye opening, verbal response, motor response; score 3-15
______ is a transient, paroxysmal, synchronous discharge of neurons in the brain
seizure
Which transient abnormalities can cause seizures?
hypoglycemia, hyponatremia, hyperthermia, intoxication - tx underlying cause
Antiepileptic drugs decrease _______ or enhance _______
decrease neuronal excitability
enhance inhibition
Which anti-seizure meds are enzyme-inducers? How do they impact anesthetics?
- Phenytoin, Tegretol, Barbiturates are enzyme-inducers
- Likely require higher doses of hepatically-cleared medications
