CNS- II Flashcards
1
Q
What is ALS?
A
- Most common motor neuron diseases causing muscular atrophy
- death of upper motor neurons (betz cells- responsible to fast conduction) and degerneration of axons/lateral corticospinal tract
- death of lower motor neurons (located in anterior horn spinal cord/brainstem)
- reactive gliosis in areas of degeneration
- affected motor units lose innervation
- progressive degerneration of axons causes loss of myelin
- nearby motor nerves may sprout axons in attempt to maintain function, but eventually nonfunctional scar tissue replaces normal neuronal tissue
2
Q
What is cause of ALS?
A
- genetic (familial ALS “FALS”) link is seen in 10-20% of all ALS cases (defects in enzyme superoxide dismutase gene)
- over 90% of cases of ALS occur randomly with no identifiable cause and no risk factors and are referred to as sporadic ALS
- Histology: protein aggregates (TDP-43) within cytoplasm of motor neurons
- provides clues, but don’t know how to interpret increased dying)
3
Q
What are some current theories for causes of ALS?
A
- Glutamate excitotoxicity- excess glutamate causes Ca to go into cell (particularly NMDA) then extra Ca causes apoptosis in the cell
- oxidative injury
- protein aggregates
- autoimmune-induced calcium influx
- viral infections
- deficiency of nerve growth factor
- trauma
- environmental toxins
Current research suggests an excess of glutamatergic signaling in the synaptic cleft
4
Q
What is the prognosis of ALS?
A
- Chronic, progressively debilitating disease- death in as little as 1 year survivial up to 10 years
- men affected 3:1, average age 50 years
5
Q
ALS signs and symptoms?
A
- Fasciculations, spasticity, atrophy, weakness, and loss of funcitoning motor units (especially in forearms and hands)
- impaired speech, chewing, and swallowing; choking; drooling
- difficulty breathing, especially if brain stem affected
- muscle atrophy
- autonomic dysfunction- as brainstem more impacted, issues with hemodynamic instability
- depression
6
Q
ALS diagnosis
A
- electromyography- abnormalities of electrical activity in involved musles
- muscle biopsy: atrophic fibers interspersed between normal fibers
- CSF analysis by lumbar punction: elevated protein levels
7
Q
ALS treatment?
A
- Riluzole: glutamate antagonist and increases glutamate reuptake<– less glutamate in cleft. decreases preogression for a couple of months
- symptomatic
- baclofen or diazepam
- gabapentin, amitriptyline- for pain
- physical therapy
- percutaneous feeding tubes
- tacheostomy
8
Q
What are seizures?
A
- abnormal electrical discharges of neurons in the brain
- transient, paroxysmal and synchronized discharges of groups of neurons
- group of neurons firing inappropriately
9
Q
Causes of seizure disorders?
A
- Half of all cases are idiopathic
- birth trauma; anoxia; perinatal infection; genetic abnormalities, such as tuberous sclerosis and phenylketonuria; perinatal injuries
- metabolic abnormalities, such as hypoglycemia, pyridoxine deficiency (Vit B6) or hypoparathyroidism
- brain tumors or other space-occupying lesions
- meingitis, encephatlitis, brain abscess
- traumatic injury
- toxins: mercury, lead or carbon monoxide
- stroke
- familial incidence in some sz disoder
10
Q
Pathophysiology of seizures?
A
- epileptogenic focus: hyperexcitable neurons depolarize more readily when stimulated
- membrane potential at rest is less negative or inhibiotry connections are missing
- may be due to decreased GABA activity or localized shifts in electrolytes
- on stimulation, epileptogenic focus fires and spreads electrical current toward the synapse and surrounding cells
- if impulse cascades on one side of brain (partial seziure) OR
- impulse can go down both sides of brain (generalized seizure) or cortical, subcortical, or brain stem areas
- Brain’s metabolic demand for oxygen increases dramatically during a seizure
- can lead to hypoxia and neuronal cell death
-
firing of inhibitory neurons causes the excitatory neurons to slow their firing and eventually stop
- if this inhibitory action doesn’t occur, the result is status epilepticus
11
Q
What is status epilepticus?
A
one prolonged seizure or a series of seziures (>2) without regaining consciousness
- may be fatal (emergency)
- using up ATP, increase anaerobic metabolism, increase CO2, and other anaerobic metabolites… eventually can cause neuronal death
- rule out hypoglycemia
- metabolic acidosis & hyperthermia often ensue requiring controlled ventilation and cooling measures
- problematic because decreasing o2 available to brain
12
Q
What is a generalized tonic clonic sezure?
A
- altered consciousness
- tonic stiffening followed by clonic muscular contractions
- tongue biting
- incontinence
- labored breathing, apnea, cyanosis
13
Q
What is an absence seizure?
A
- change in level of awareness
- blank stare
- automatisms (purposeless motor activity)
14
Q
What are atonic seizures?
A
sudden loss of postural tone
temporary loss of alertness
15
Q
What are myoclonic seizures?
A
brief muscle contractions that appear as jerks or twitching
16
Q
What shows on EEG for seizure diagnosis?
A
- Tonic-clonic seizures, high, fast, voltage spieks are present in all leads
- absence seizures. rounded spike wave complexes are diagnostic
- a negative EEG doesn’t rule out epilepsy because the abnormalities occur intermittently
17
Q
What is treatment for seizures?
What are the big drug s/e?
What’s given for generalized tonic/clonic or complex partial seziures?
What’s given for absence seizures?
Surgeries to treat seizures?
A
- multiple drugs sometimes required for control
- drugs have many interactions and toxic effects
- examples: sedation (all), adverse hematologic reactions, rashes, developmental delay
- drug therapy speicfic to the type of seizure, including phenytoin, carbamazepine, phenobarb, for generalized tonic-clonic seizures and complex partial seizures
- VPA, clonazpam for absence seizures
- surgical removal of demonstrated focal lesion, if drug therapy is ineffective: temporal lobectomy
- may have residual hemiparesis
- surgery to remove the underlying cuase, such as tumor, abscess, or vascular problem
- vagal nerve stimulator implant: may have hoarsenss
- IV diazepam, lorazepam, phenytoin, or phenobarb for status epilepticus
- administration of dextrose (when seizures secondary to hypoglycemia) or thiamine (in chornic alcholism or withdrawal)
18
Q
What is normal CBF?
A
- Intact autoregulation= normal CBF 50 mL/100 g brain tissue per minute
- 1500 g brain with normal CO (5L/min)= CBF 750 mL/min
- 15% of cardiac output
- CBF is autoregulated
19
Q
What is normal CRMO?
A
- CRMO= 250 mL/min
- 18-23% of total body oxygen consumption
- CMRO can be decreased by temp reducitons and various anesthetic agents
- CMRO increased by temperature increases and seizures
20
Q
How much does CBF increase for every 1 mmHg increase in PaCO2?
A
CBF increase by 1-2 mL/100g/min for every 1 mmHg increase in PaCO2
- Decrease occurs during hypocarbia, so that CBF is decreased by approximately 50% when PaCO2 is acutely reduced to 20 mmHg
- 6 hours: return of CSF pH to normal; hypocarbia no longer able ot significantly reduce CBF
21
Q
What happens when Pao2 is <50 mmHg?
A
- Cerebral vasodilation and increased CBF
- “hail mary”
22
Q
What is normal ICP? What is it determined by? When can it increase?
A
- Normal 5-15 mmHg
- Determined by
- rigid cranial vault fixed volume (total 1200-1500 mL)
- brain (cellular and ICF) (80%)
- `hyperosmotic diuretic to get rid fo fluid
- blood (arterial and venous) (12%)
- if compressing jugular vein, increase vneous back up into head and increase venous blood volume
- never want blood vessels dilated because increase volume
- CSF (8%)
- brain (cellular and ICF) (80%)
- rigid cranial vault fixed volume (total 1200-1500 mL)
- Increase ICP with intracranial bleeding, hydrocephalus, tumor, edema, following traumatic injury, etc
- with brian injury, increase blood and increase brain edema problematic
- if brain expands, compresses agaisnt bone/dura mater
23
Q
What is CPP?
A
- Cerebral perfusion pressure= MAP- ICP (or cvp, whichever is greater)
- Normal is 80-100 mmHg
- CPP < than 50 mmHg- slowing seen on EEG
- CPP between 25-40 flat EEG
- CPP <25 mmHg sustained = irreversible brain damage
- variables affecting CBF during anesthesia: PaO2 AND PaCO2, systemic blood pressure, ICP, cerebral autoregulation and various drugs
24
Q
Management of increased ICP?
A
Maintain CPP and cerebral blood flow (decrease ICP <20 mmhg and increase BP)
- Mannitol (0.25-0.5 g/kg)/hypertonic saline 1-2 mL/kg over 5 minutes
- furosemide
- vasopressors- if increased ICP, then you need to maintain arterial BP high enough to ensure blood flow to brain! (think CPP= MAP-ICP!)
- PaCO2= low normal 30-35 mmHg (6 hours)
- maintain normothermia
- barbiturate/propofol coma- get EEG down to almost flat to bring O2 demand down. Allows all O2 in brain to go towards housekeeping/normal integrity
- CSF drainage if available (ventriculostomy)
- HOB 30 degrees- encourage venous outflow
- Corticosteroids (only in brain tumor patients)
- Surgical decompression and/or craniecromt (TRAUMA)
25
Q
What is herniation?
A
- extreme result of increased ICP
- Various types of herniation syndromes are categorizes based on region of brain affected
- severe ICP elevation leads to decreased levels of consciousness and coma
- acute increases in ICP may not be tolerated as well as chronic intracranial HTN
26
Q
What happens with subfalcine herniation?
A
- primary motor cortex compression of anterior cerebral artery
- aka- herniation of cingulate gyrus under the falx cerebri
27
Q
What happens with transtentorial herniation?
A
- this is a herniation of contents over the tentorium cerebelli
- causes posterior cerebral artery compression
- can see pupillary dilation on affected side and loss of reflexes
- issue with vision
28
Q
What is herniation of cerebellar tonsils?
A
- herniation through foramen magnum
- loss of CV control, arousal, respiratory symptoms
- life ending damage to basal structures
29
Q
What is normal volume capacity of brain and spinal cord?
A
1600-1700 mL
30
Q
How much CSF in cranial vault at any time?
Rate of CSF production?
WHat forms CSF? Absorbs CSF?
A
- 100-150 mL CSF at any one time in cranial vault
- CSF produced at constant rate of 500-600mL/day or 20-25mL/hour
- CSF formed from choroid plexus secretion and passage of substances across BBB
- CSF reabsorbe by arachnoid villi and arachnoid granulations- function like one way valves
- fluid flows when CSF pressure is 1.5mmHg > than venous pressure
31
Q
What is communicating hydrocephalus? Non communicating?
A
- Communicating hydrocephalus= free flow through ventricles
-
no obstruction but problem with arachnoid villi
- will need shunt
- also seen infection with WBC/RBC clogging smaller arachnoid villi
-
no obstruction but problem with arachnoid villi
- non-communicating= flow out of one or more ventricles is blocked
- d/t tumor osbstructing flow, or big lesion blocking flow through the ventricles
32
Q
Causes of hydrocephalus?
A
- Disease (such as meningitis), tumors, traumatic head injury, subarachnoid hemorrhage blocking exit from ventricles to cisterns
- genetic inheritance (aqueductal stenosis)
- developmental disorders such as those associated with neural tube defects, including spina biida and encephalocele
- complications of premature birht such as intraventricular hemorrhage
33
Q
Hydrocephalus symptoms in infants?
A
- increased head cirucmference
- vomiting
- sleepiness
- irritability
- downward deviation of the eye (also called sunsetting)
- seizures
34
Q
Hydrocephalus symptoms in adult and older children?
A
- HA
- vomiting
- nausea
- pappilledema (swelling of optic disk that’s part of optic nerve)
- blurred vision; diplopia
- sunsetting of eyes
- problems with balance, poor coordination
- gait disturbance
- slowing of loss of development
- lethargy; drowsiness
- irritabiity
- other changes in personality or cognition, including memory loss
35
Q
What is a CVA?
A
- Sudden onset of neurological deficits or symptoms devleoping over several minutes to hours
- 80-85% thrombotic events while 15-20% hemorrhagic
- Both lead to ichemia
- cerebral infarctions occur as cells die from lack of oxygen and nutrients
- injury to surrounding cells disrupts metabolism and leads to changes in ionic transport, localized acidosis and free radical formation
- Ca, Na, and water accumulate in injured cells, and excitatory NT (such as glutamate- signaling apoptosis) are released
- continued cellular injury and swelling may cause further damage
*
36
Q
What do clinical features of stroke depend on?
A
- clinical features of stroke vary according to affected artery and extent of collateral circulation
- stroke in one hemisphere causes s/s on the opposite side of the body
- storke that damages cranial nerves affects sturctures on same side
37
Q
What are some cuases of stroke?
A
- Systemic hypoperfusion (cardiac arrest, hypotension)
- embolism (far, air, blood clot)
- thrombosis (often preceded by TIA)
- cerebral atherosclerosis most common cause of ischemic stroke (DM, HTN, smoking)
- SAH (trauma, hypertension, coagulopathy, aneurysm)
- Intracerebral/brain parenchymal hemorrhage (trauma, HTN, coagulopathy, open heart sx)
- open heart d/t heparin admin on bypass
38
Q
What can happen with anterior cerebral artery injury?
A
contralateral leg weakness
39
Q
What injury can be seen with middle cerebral artery stroke?
A
- contralateral hemiparesis and hemisensory deficit (face and arm more than leg)
- aphasia (dominant hemisphere)
- contralateral visual field defect
40
Q
What are symptoms with posterior cerebral artery stroke?
A
contralateral visual field defect
41
Q
What can be seen with stroke in penetrating arteries
A
contralateral hemiparesis and hemisensory defects
42
Q
What are defects seen with basilar artery stroke?
A
- oculomotor deficits
- ataxia with sensory and motor defects
43
Q
What defects are seen with vertebral artery stroke?
A
- Lower cranial nerve deficits and or ataxia with sensory deficits
44
Q
What are some variables that influence the extent of injury with strokes?
A
- Site of occlusion
- collateral circulation
- perfusion pressure- want high normal pressure to optimize collateral flow
- time course of occlusive event
45
Q
How do we diagnosis strokes?
A
- Non-contrast CT scan ID’s evidence of hemorrhagic stroke (lesions larger than 1 cm) immediately
- an ischemic stroke will be apparent within first 72 hours of symptom onset
- MRI- assists in id’ing areas of ischemia or infarction and cerebral swelling
- arteriogrpahy- where disruption in cerebral circulation by occlusion (such as stenosis, acute thrombus, or by hemorrhage)
- carotid duplex scan- id the degree of stenosis
- echo- reveals thrombi within the atrium or ventricle
46
Q
What are soe risk factors, onset, s/s of systemic hypoperfusion stroke substype?
A
- Risk factors- hypotension, hemorrhage, cardiac arrest
- onset- parallels risk factors
- s/s
- pallor
- diaphoresis
- hypotension
47
Q
What is main difference b/w embolic and thrombotic stroke s/s?
A
embolic- sudden
thrombotic- often preceded by TIA
otherwise, risk factors, s/s similar
48
Q
What is main difference b/w subarachnoid hemorrhage and intracerebral hemorrhage?
A
Subarachnoid hemorrhage often occurs during exertion
intracerebral hemorrhage is a gradaully progressive onset
- Both have s/s of HA, vomiting
- transient LOC ( SAH)
- Decreased LOC (ICH)
- Risk factors for both are HTN, coagulopathy, drugs, trauma
49
Q
What are some causes of ischemic stroke?
A
- Cardioembolism
- large vessel atherosclerotic narrowing
- small vessel occlusiv edx (DM, HTN)
- Hyperocoaguable state
50
Q
Risk factors ischemic stroke?
A
- # 1 systemic hypertension
- others: smoking, HLD, DM, ETOH (>6 /day), increased homocysteine level
51
Q
Management of ischemic stroke?
A
- ICP, CPP and cerebral edema management
- at risk for malignant middle cerebral artery syndrome
- edematous infarcted tissue compresses anterior and posteiror cerebral artieres causing secondary injury
- at risk for infarction of cerebellum with basillar artery compression and brain stem ischemia
52
Q
What is the ischemic penumbra?
A
- Potentially viable tissue
- area around impacted by stroke, brain tumor, TBI etc
- specturm of injured neurons when CBF is interrupted as a result of vessel occlusion
- in the affected area, there is a core of irreversibly damaged neurons, surrounded by an area of electrically silent, but viable neurons known as the ichemic penumbra
- the silent neurons may survive for hours, although exact duration is unknown
53
Q
How can we increase survivability of ichemic penumbra?
A
- Hyperthermia of 1-2 degress C and serum hyperglycemia have been shown to accelerate cell death
- restoration of CBF to the penumbra within critical hours may salvage viable neurons and minimize neuro deficit
- without intervention, core of the infarcted territory will subsume the penumbra
54
Q
Treatment for ischemic stroke?
A
- Thrombolytic therapy with TPA within 4.5 hours after onset of symptoms
- may exceed time limit in certain populations- over last couple of years, studies have suggested window up to 24 hours (the earlier the better)
- ASA, warfarin, heparin
- CEA- done preventatively with stenosis >70% - (definitive proof to prevent strokes)
- angioplasty and stents
- surgical decompression/cerebellar resection may be needed as lifesaving measures
55
Q
What is hemorrhagic stroke?
A
- usually secondary to aneurysms at the circle of willis with involvement of ant and post communicating arteries
- systemic HTN, DM, cigarette smoking increase rupture risk
- size of aneurysm is important 6-10 mm at greatest risk of rupture
- >25 mm 5% risk of rupture /year + mass effect can cause symptoms
- 4x the risk of death c/t ischemic stroke
- high incidence among African Americans
- Volume of blood and LOC determine prognosis
- often decompensate 24-48 hours after bleed s/t edema formation
56
Q
Diagnosis for hemorrhagic stroke?
A
Symptoms warrant non-contrast CT
- Worst HA of my life
- photophobia
- stiff neck
- decreased LOC
- focal neuro changes
- ECG changes- huge SNS release
- CT scan shows subarachnoid blood
57
Q
What is treatment of hemorrhagic stroke?
A
- early diagnosis and intervention (coiling/clipping within 72 hours) improve outcomes
- ICP control is important
- supportive therapy- ETT, ICP monitor, systolic <130, sedation, etc
- BP management critical CPP 61-80mmHg
- too high- rebleed
- too low- ischemia to penumbra
- High incidence vasospasm 3-15 days following insult
58
Q
What are some types of injury in TBI?
A
- Diffuse axonal injury- tear axons
- traumatic subarachnoid hemorrhage
- coup-contrecoup injureis
- brain floating–> blow to head, brain slams to front of cranium, then richochet back
- cortical contusions and lacerations
- subdural, epidural or intracerebral hematoma
59
Q
What is TBI patho?
A
- Primary injury
- biomechanical effect of force applied to skull and brain (ms)
- coup and countercoup contusion
- lacerations
- diffuse axonal injury
- biomechanical effect of force applied to skull and brain (ms)
- Secondary injury (goal= prevention)
- ishcemia, brain swelling, edema, intracranial hemorrhag, increased ICP, herniation (minutes to hours)
- aggrevating factors= hypoxia, hypercarbia, hypotension, anemia, hyperglycemia, sz, infection
60
Q
What is an epidural hematoma?
A
- worst kind of bleed you can have
- arterial bleeding b/w skull and dura
- usually related to meningeal artery rupture s/t skull fracture
- dx by CT and clinical signs an symptoms
-
LOC followed by lucid honeymoon period, followed by sudden decompensation
- hemiparesis, mydriasis, and bradycardia reflex uncal herniation and brain stem compression
- treatment is PROMT burr holes at fracture sites
61
Q
Subdural hematoma?
acute vs chronic?
dx?
symptoms?
txmt?
A
- Lacerated or torn bridging veins that bleed b/w dura and arachnoid
- chronic= spontaneous or follows relatively minor head truama in elderly, HD or anticoagulated pt
- Acute= whip lash, shaken baby syndrome
- clinical dx verified by CT scan
-
symptoms develop over first 48 hours or ven severy days (venous= slow bleed puts pressure on adjacent brain tissue) and wax and wane
- HA, drowsiness, obtundation at first followed by hemiparesis, hemianopsia, dififculties with language/dementia
- conservative medical mgmt in stable pt
- surgical removal of clot is symptoms progressivey worse
- normocapnia preferred
62
Q
Intracranial tumors?
A
- tumor= space occupying lesion which destorys, relocates and compresses local tissue (localized edema) can also obstrcut CSF flow
- even histologically “benign” tumor is not benign if it’s in critical anatomic location
- Primary vs metastatic
- 20% all pediatric cancer
- May arise from
- meningeal layers
- CNS cells (glial, neurons, chroid plexus)
- cells housed in skull
- metastasis
- Ionizing radiation increases risk
- Peds: more infratentorial- critical centers can be compressed
- Adults: more supratentorial (glioma, mingiomas, pituitary adenomas, acoustic neuromas, metastatic tumors)
63
Q
What can gliomas secrete?
A
can secrete tons of glutamate, kills nuerons wth cytotoxicity
glioma compresses and actively destorys tissue as they grow
64
Q
What are sx of intracranial tumors?
A
- Sx depend on area affects
- most symptoms r/t increased ICP
- HA
- n/v
- neuro changes
- sz
- increased BP and decreased HR
- Loss of autoregulation in blood vessels surrounding intracranial tumors leads to maximum vasodilation
- blood flow becomes pressure dependent in these area
65
Q
What is treatment for intracranial tumors?
A
- treatment option depend on diagnosis
- ICP mgmt and contorl of seizures until definitive mgmt; steroids for cerebral edema
- steroids improve vasogenic edema and improve neuro sx withi 12-36 hours in many brain tumor patients
- option
- surgey- dx/decompressive/curative
- radiation therapy- gamma knife;
- brachytherapy- sterotacti implantaiton of radiation soruce for 4-6 days (glioblastoma)
- chemotherapy
- immunotherapy
- oncolytic virotherapy
66
Q
What are meningiomas?
A
- arise from mennges so the tumors are mostly located at border of brain
- often have blood supply from external carotid arteries
- mostly benign and slow growing
- surgical removal is possible
- good prognosis but recurrence is possible
- dangerous if large d/t compressive effect on healthy tissue
67
Q
What are glioblastomas?
A
- blioblastomas arise from astrocytes
- star-shaped cells that support the neurons
- high reproducing rate and support of blood vessels
- highly malignant
- fast growht also leads to decrease of o2 supply in the tumor center and tumor often develops a necrotic center
- invasive behavior with diffuse borders
-
9 month life expectancy
- some recent devleopment with immunotherapy but can someties make patients worse d/t immune resposne
68
Q
What are nonfunctioning pituitary tumors?
A
- chromophobe adenomas, craniopharyngiomas, meningiomas
- dx when large and causing symptoms by impinging on adjacent structures
- most common neuro symptoms in pt with pituitary adenomas are HA and visual changes
69
Q
What are functioning pituitary tumors?
A
- prolactinomas followed by GH and ACTH- secreting adenomas
- diagnosed when small. symptoms r/t prodcution of exces of 1 or more anterior pituitary hormones
- endocrine status must be addressed
- 1) panhypopituitarism: hypocortisolism and hyponatremia; hypotyroid etc
- 2)acromegaly- airway alteration
- 3) cushing’s disease: DM, hyperaldosteronism (hypokalemia and metabolic acidosis), HTN, CHF, obesity
