Class 8 chapter 37 Flashcards
(68 cards)
1
Q
Hypoxia and Ischemic Injury
A
Focal cerebral ischemia
Global ischemia
2
Q
Focal Cerebral Ischemia
A
Short term
Typical causes - thrombus/embolism
“Zone of penumbra” without infarction
3
Q
Global Ischemia
A
Loss of Consciousness
Release of “excitatory” amino acid neurotransmitters
Disruption of calcium balance
Formation of free radicals
Mitochondrial injury
ATP malfunction = “power failure” = edema
4
Q
Vulnerable Areas in the Brain
A
“Water-shed” areas
- At limits of cerebral blood flow
- Fragile, vulnerable
- Result in focal defects
Segments of short arteries supplying cerebral cortex = Laminar necrosis
5
Q
Excitatory Amino Acid Injury
A
Neuron injury results in release and activation of mediators that overstimulate cell receptors
- Amino acids (glutamate), catecholamines, free radicals etc
Glutamate attaches and opens calcium channels leading to “calcium cascade” into cells
- Protein breakdown
- Free radical formation
- DNA fragmentation
- Mitochondrial injury
- Cell death
6
Q
Cerebral Edema
A
Vasogenic (vessel)
Cytotoxic
7
Q
Vasogenic cerebral edema
A
Leaking of water/proteins into ISS (interstitial space)
Causes: hemorrhage, meningitis, injury, tumours
White matter more so (not as dense as gray – more blood vessels)
Result: herniation, focal defects, increased ICP (intracranial pressure), altered LOC
8
Q
Cytotoxic cerebral edema
A
Increased ICF (intracellular fluid) Causes: water intoxication, impaired K/Na pump Result: cell rupture with damage to surrounding tissue, increased ICP
9
Q
Monro-Kellie Hypothesis
A
Tissue - 80% (most stable) Blood - 10% (less stable) CSF - 10% (less stable) Compliance! An increase in one will cause a decrease in the other
10
Q
Increased Intracranial Pressure (ICP)
A
Compartment syndrome in the skull
- Intracranial pressure greater than arterial blood pressure
- Arteries collapse; blood flow to brain cut off
Compliance = change in volume (divided by) change in pressure
Tissue: tumour, edema, bleed
Blood: vasodilation, obstruction of outflow
CSF: increased production, decreased absorption, obstruction
Results in hypoperfusion, hypoxia, cell damage = decreased LOC, coma
Cushing Reflex – late signs of ICP
- Hypertension
- Widening pulse pressure
- Reflex bradycardia
Treatment - decreasing CO2 levels (vasodilator)
11
Q
Increased Intracranial Pressure (ICP) manifestations
A
Changes in LOC Papilledema Impaired eye movement Decreased sensory/motor function Vomiting Headache Pupillary changes Changes in VS (increased BP, decreased P, changes in reap pattern) Infants - bulging fontanels, cranial suture separation, increased head circumference, high pitched cry
12
Q
Brain Herniation
A
Increased intracranial pressure pushes the brain out of position
Brain tissue is compressed into the center of the brain, against bone or against rigid folds of the dura mater
Compression of the oculomotor nerve is an early sign
13
Q
Hydrocephalus
A
Increased CSF volume enlarges ventricles and compresses brain tissue
Non-communicating/Obstructive
- Congenital malformations, tumors, inflammation, hemorrhage = CSF blockage
Communicating
- Impaired reabsorption of CSF via arachnoid villi d/t infection, scarring, blockage by lyzed RBCs post repair of bleed
- Increased production of CSF (rare)
Manifestations
- Fontanel bulging fetus/newborn
- Signs of increased ICP in all ages
- Optic nerve atrophy/blindness
14
Q
Traumatic Brain Injury
A
Primary/Direct injuries
- D/t impact
- Microscopic damage: diffuse axonal injury
- Contusions (coup - brain hits front of skull, countercoup - brain hits back of skull)
Secondary injuries - D/t: Ischemia (most common) Hemorrhage Infection Increased intracranial pressure
15
Q
Traumatic Brain Injury types
A
- Mild
Concussion (immediate & possible post-concussion syndrome)
Limited symptoms to momentary LOC, residual amnesia - Moderate
Small hemorrhages, edema
LOC, cognitive/motor deficits, hemiparesis, nerve palsies - Severe
Shearing, pressure = axon/vessel/tissue damage
Extensive damage with secondary manifestations (Hemiplegia, signs of elevated ICP, coma)
16
Q
Hematoma - Epidural
A
Meningeal artery tear
- Rapid bleeding; unconsciousness may be followed by brief lucid period
- Ipsilateral pupil dilation, contralateral hemiparesis d/t uncal herniation (push down to brain stem)
- Treatment prior to LOC has good prognosis
17
Q
Hematoma - Subdural
A
Venous tear between dura & arachnoid
Slower bleeding
1. Acute (within 24 hours)
Increased ICP, decerebrate posturing, LOC, high mortality rate
2. Subacute (2-10 days)
Periods of improvement prior to rapid deterioration
3. Chronic (weeks)
Slow bleed, decreased LOC, drowsiness, confusion, apathy, headache
18
Q
Hematoma – Intracerebral (Traumatic)
A
Usually frontal or temporal lobes Risk: age, alcoholism Symptoms dependent on size and location Increased ICP Herniation
19
Q
Diffuse Brain Injury Signs
A
- Doll’s eye response (vestibulo-ocular reflex)
- Indicates brain stem damage
- Possible tentorial herniation
Abnormal posturing
- Decorticate posturing
- Damage to one or both corticospinal tracts involving the “red nucleus” (motor movement) in midbrain
- Arms flexed
- Legs extend with feet turned inward - Decerebrate posturing
- Indicates brain stem damage bwloe level of red nucleus
- Upper and lower extremity extension
- Head arched back
- Can be one side or both or just arms - Cheyne-Stokes
20
Q
Brain Attack (CVS/Stroke) Risk Factors
A
- Ischemic Stroke (interruption in blood flow)
- Age, gender, race, familial, HTN, smoking, DM, sickle cell disease, atrial fibrillation, CAD
- Obesity, physical inactivity, alcohol, drug use, hypercoagulability disorders, oral contraceptives, hormone replacement therapy - Hemorrhagic Stroke (bleed into brain tissue)
- Htn, aneurysms, AV malformations, head injury, blood dyscrasias
21
Q
Transient Ischemic Attack (TIA)
A
Focal cerebral ischemia “zone of penumbra” without infarction Reverses prior to ischemia Similar risk factors and symptoms as stroke but symptoms last < 1 hour with fully recovery Increases risk of stroke
22
Q
Manifestations of Acute Stroke
A
Usually unilateral and focal Always sudden Weakness/numbness (face, arm, leg) Vision loss Aphasia (language disorder) Dysarthria (motor speech disorder) Ataxia (muscle coordination disorder)
23
Q
Aneurysmal Subarachnoid Hemorrhage
A
- Pre-rupture
- Sudden-onset headache with nausea and vomiting, dizziness - Hemorrhage
- Sudden severe headache, N/V, nuchal rigidity (neck), photophobia, vision and motor problems, LOC - Complications post-op
- Rebleeding, vasospasm, hydrocephalus
24
Q
Risk factors of rupture
A
Age Smoking HTN Alcoholism Size of aneurysm Conditions that increase ICP
25
Arteriovenous Malformations
Tangle of abnormal arteries and veins linked by fistulas
- Possibly due to lack of capillary formation
- Structurally unstable with high pressure flow from arteries to veins
- Ischemic symptoms
Symptoms may not show until > 40 years of age
Hemorrhage usually slower process
Surgical removal
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Acute Bacterial Meningitis
Inflammation of pia, arachnoid and subarachnoid
Contagious (direct contact – blood/mucous)
Carriers
10% permanent damage (ear, sight)
10% fatal
Neisseria meningitidis or Streptococcus pneumoniae
Group B streptococci (neonates)
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Acute Bacterial Meningitis risk factors
```
Basilar skull fracture
Otitis media
Sinusitis/mastoiditis
Neurosurgery
Sepsis
Living in close quarters/aged/infants
```
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Acute Bacterial Meningitis patho
Bacteria replicate and lyze in CSF
Endotoxins/debris result in inflammatory process
Neutrophils/albumin allowed in CSF
Thrombi, scarring, blockage
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Acute Bacterial Meningitis manifestations
Headache, fever, nuchal rigidity
N/V, photophobia, altered mentation
Petechial rash/palpable purpura (N. meningitides)
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Acute Bacterial Meningitis manifestations
Headache, fever, nuchal rigidity
N/V, photophobia, altered mentation
Petechial rash/palpable purpura (N. meningitides)
Seizures, cranial nerve palsies, focal cerebral signs
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Acute Bacterial Meningitis diagnosis
Lumbar puncture - cloudy, purulent
Kernig sign
- Resistance to extension of knee while lying with hip flexed
Brudzinski sign
- Flexion of neck induces flex of hip/knees
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Acute Bacterial Meningitis treatment
Antibiotics
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Viral Meningitis
Acute lymphocytic
Enteroviruses, Epstein-Barr virus, mumps virus, HSV, West Nile
Similar to bacterial but less severe
CSF has lymphocytes and small amounts of protein only, normal sugar
Self-limiting unless herpes simplex virus type 2 (HSV-2) which requires acyclovir
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Encephalitis
Parenchymal infection of brain or spinal cord
Usually viral
- HSV
- West Nile
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Encephalitis manifestations
Lethargy, disorientation
Fever, headache, nuchal rigidity
Seizures, paralysis, delirium, coma
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Encephalitis diagnosis
Lumbar puncture
| CSF investigation
37
Brain Tumors
Most often secondary site of metastasis
Primary more common in children (mortality rate 45%)
Risks:
Rarely benign, but if so, still dangerous
- Pressure
- Attachment = difficult to excise
Neurogliomas of astrocytic origin most common in adults
Medulloblastomas most common in children
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Neuroglial Tumors
Most common primary tumor
Graded I to IV
Astrocytes: protective neurons, supply nutrients/oxygen
Oligodendrocytes: supportive cells in brain, ex form myelin
Ependyomal: line ventricles & spinal cord
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Astrocyte
1. Infiltrating (middle adult)
Usually cerebral hemispheres
Focal deficits, headache, seizures
2. Non-infiltrating (children)
Usually cerebellum, 3rd ventricle
Slow growth, minimal symptoms, easily resected
40
Oligodendroglioma
Middle adult
Usually cerebral hemispheres white matter
Unpredictable, prone to hemorrhage
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Ependymoma
Young adult
Epithelial lining of 4th ventricle/spinal canal
Hydrocephalus, increased ICP
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Medulloblastoma
Originates in neurons of cerebullum, posterior fossa
Fast growing, spreads via CSF to brain/spine
Appears in infants, young children
Manifestations include signs of increased ICP
Highly malignant, but radiosensitive and excisable
43
Meningiomas
Outside brain, grows slowly
Older adult
Usually benign and excisable
44
Primary central nervous system lymphomas
Increased incidence of late
Common in immunocompromised
B-cell origin (lymphocytic)
Invasive, diffuse, aggressive
45
Metastatic tumors
Melanomas to frontal & temporal lobes
Breast cancer to cerebellum and basal ganglia
NSC (non small cell) lung cancer to occipital lobe
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Brain Tumor Manifestations
```
Dependent on location and size
Vasogenic edema/papilledema/increased ICP
Headache - distinctive characteristics
- In morning
- Improves with elevation of head
- Worse with sudden head movements
- Doesn’t respond to usual medications
- Accompanied by N/V
```
47
Diagnosis of Brain Tumors
MRI as CT unreliable
EEG
Cerebral angiogram
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Treatment of brain tumours
Surgery
Irradiation
Chemotherapy
49
Seizure Disorders
Temporary alterations in cerebral activity
Causes are numerous
```
1. Provoked = seizure
Fever (children)
Metabolic condition (adults)
Structural changes
Cellular changes
```
2. Unprovoked/idiopathic = epilepsy
Genetic
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Partial Seizures
Simple Partial/Elementary
Complex Partial
Secondarily Generalized Partial
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Simple Partial/Elementary seizures
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One hemisphere only
No LOC
Symptoms dependent on area involved
May cause “Jacksonian march”
Sensory symptoms may be only sign
No observable symptoms
Prodrome/aura is not just a warning!
ANS involvement (tachycardia, diaphoresis, hypo/hypertension, pupil changes)
```
52
Complex Partial
```
Often temporal lobe
Altered consciousness
Hallucinations, déjà vu, idea flood, fear, etc.
Automatisms
Repetitive non-purposeful movements
Confusion after is common
```
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Secondarily Generalized Partial
Focal onset but generalized
| Tonic/clonic activity, may have aura
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Generalized Seizures
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Absence (“petit mal”)
Atonic (“drop attacks”)
Myoclonic
Tonic-Clonic (“grand mal”)
Status Epilepticus
```
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Absence seizure
Generalized disturbance of consciousness
Blank stare, often motionless or automatisms
Lasts only seconds so can be overlooked
“Atypical” type has slow onset/end
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Atonic seizures
Sudden loss of muscle tone
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Myoclonic seizures
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Brief muscle contractions bilaterally
Face, trunk or one or more extremities
Tonic
- Rigid, violent contractions or
Clonic
- Repeated contraction/relaxation
```
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Tonic-Clonic seizures
1. Tonic Phase
- Extension of extremities, LOC, incontinence, cyanosis
2. Clonic Phase
- Rhythmic contraction/relaxation
3. Postictal Phase
- Return to consciousness once RAS (wake/sleep center) function
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Status Epilepticus
Seizure activity that doesn’t cease on own or occurs successively
High mortality rate
Must treat cause
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Dementia
```
Permanent brain damage resulting in impaired memory and cognition
- Short and long-term memory
- Abstract thinking
- Judgement
- Personality changes
Alzheimer Disease
Vascular Dementia
Frontotemporal Dementia
Creutzfeldt Jakob Disease
Wenicke-Korsakoff Syndreom
Huntington Disease
```
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Alzheimer Disease
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40% of 85 year olds
Genetic, familial or sporadic
Death in 8 years (average)
Diffuse degeneration/atrophy of cerebral cortex
Enlargement of ventricles
```
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Alzheimer Disease – pathological processes
1. Neuritic (senile) plaques
- Accumulation of amyloid peptide
- Degenerative nerve terminals with an amyloid core
2. Neurofibrillary tangles
- Helical fibrous proteins
3. Decreased enzyme that synthesizes acetylcholine
- Neurotransmitter associated with memory
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Manifestations of Alzheimer's
1. Initial: subtle
Loss of memory and denial of shame
Mild personality change – withdrawal/loss of sense of humour
```
2. Moderate stage
Loss of higher cortical functions (problem solving)
Depression if aware of changes
Hostility
Sundown syndrome
```
3. Late stage
Loss of ability to respond to environment/family
Incontinence
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Vascular Dementia
Ischemic or hemorrhagic damage (MI, arrhythymias, DM, PVD, infection, smoking)
Slow psychomotor functioning
Depression is common
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Frontotemporal Dementia (Pick)
Atrophy of frontal and temporal lobes
- Progressive syndrome
Behavioral changes common
- Impulsiveness, loss of inhibitions (social behaviour), apathy
Language/understanding issues are less common but do happen
Death d/t infection in 2-10 years
Diagnosis: Neuroimaging
66
Creutzfeldt Jakob Disease (mad cow)
Rapid, infective protein “prion” (protein)
Bovine spongiform encephalopathy (BSE)
- “Mad cow disease”
Dementia within 6 months of infection
Results in degeneration of pyramidal and extrapyramidal systems
```
Personality changes
Visual/spatial coordination issues
Impaired memory and judgement
Extreme dementia
Insomnia
Ataxia
Death in months
```
67
Wernicke-Korsakoff Syndrome
```
Cause is typically thiamine deficiency as a result of chronic alcoholism
Manifestations:
- Weakness of eye muscles
- Delirium, confusion, hallucinations
- Memory loss with confabulation
- Polyneuritis
```
Physical symptoms are somewhat reversible with nutrition, thiamine, but not “psychosis”
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Huntington Disease
Cause is hereditary
Emerges in 40-50’s
Cell death in basal ganglia motor control
Manifestations
- Chronic progressive chorea (rhythmic movement)/ dyskinesia (inability to control movement)
- Psychological changes
- Cognitive decline, dementia
