Neuro Pathophysiology PPT Flashcards
(145 cards)
1
Q
DSM-5 Criteria to diagnose dementia:
* Significant _____ decline from the ______ level
of performance in one or more cognitive domains
* Interferes with _____
* Does not occur exclusively in the context of a
delirium
* Not better explained by any other ______ or _________ condition
A
DSM-5 Criteria to diagnose dementia:
* Significant cognitive decline from the baseline level
of performance in one or more cognitive domains
* Interferes with the activities of daily living
* Does not occur exclusively in the context of a
delirium
* Not better explained by any other medical or
psychiatric condition
2
Q
DSM-5 Criteria for delirium:
* Disturbance in _____ & _______
* Develops ______ and tends to ______
in severity.
* At least one additional disturbance in
cognition
* Not better explained by _______ ________
* Do not occur in the context of a
severely reduced level of arousal or
coma
* Evidence of an ______ _________
A
DSM-5 Criteria for delirium:
* Disturbance in attention & awareness
* Develops acutely and tends to fluctuate
in severity.
* At least one additional disturbance in
cognition
* Not better explained by preexisting
dementia.
* Do not occur in the context of a
severely reduced level of arousal or
coma
* Evidence of an underlying organic
cause or causes
3
Q
Pathophysiology of Major Neurocognitive Disorder:
Accumulation of native _____ in the brain
(except vascular)
A
Pathophysiology of Major Neurocognitive Disorder:
Accumulation of native proteins in the brain
(except vascular)
4
Q
Vascular dementia ~____% of all dementia cases
* Incidence increases with ___
* Doubles every _____ years
* Risk factors (4):
A
Vascular dementia ~15% of all dementia cases
* Incidence increases with age
* Doubles every 5.3 years
* Risk factors - hypercholesteremia, diabetes
mellitus, hypertension, and smoking
5
Q
Lewy body dementia ___% of dementia cases
A
Lewy body dementia: ~5% of dementia cases
6
Q
Parkinson disease dementia ___% of cases of
dementia
A
- Parkinson disease dementia 10% of cases of
dementia
7
Q
Frontotemporal dementia ~___% of dementia
cases in patients older than ____ years of age
A
Frontotemporal dementia ~25% of dementia
cases in patients older than 65 years of age
8
Q
Dementia-type diseases:
Cause _______ damage to various areas of your brain, causing _______ in
several areas of the brain to die
A
Dementia-type diseases:
Cause progressive damage to various areas of your brain, causing neurons in
several areas of the brain to die
9
Q
Dementia-type diseases: (5)
A
- Alzheimer’s disease
- Frontotemporal dementia
- Chronic traumatic encephalopathy (CTE)
- Lewy body dementia
- Limbic predominant age-related TDP-43 encephalopathy
(LATE)
10
Q
Alzheimer’s
Disease:
Premature aging of the brain Alzheimer disease is the most common cause of
dementia, ___ to ___% of all
cases of dementia.
Number is projected to double every ____ years and will increase to reach ____ million by 2050.
Characterized by a _______ decline in ______ and
_________ in personal daily activities.
A
Alzheimer’s
Disease:
Premature aging of the brain
Alzheimer disease is the most common cause of
dementia - 70 to 80% of all
cases of dementia.
Number is projected to double every 5 years and will
increase to reach 152 million by 2050.
Characterized by:
progressive decline in thinking and
independence in personal daily activities.
11
Q
Vitamin ____ deficiency is associated with neurologic problems.
A special marker of vit. B12 deficiency is elevated _________ levels, which can cause brain damage by oxidative
stress, increasing _____ influx and ______.
A
Vitamin B12 deficiency is associated with neurologic problems.
A special marker of vit. B12
deficiency is elevated homocysteine levels, which can cause brain damage by oxidative stress, increasing calcium influx and apoptosis.
12
Q
The National Institute on Aging—
Alzheimer’s Association
(updated the 1984 NINCDS-ADRDA criteria for
higher specificity and sensitivity)
- Positive lesions (due to __________),
characterized by the
_________ of __________ tangles,
_________ plaques, dystrophic neurites, neuropil threads, and other deposits found in the brains - Negative lesions (due to _____), that are characterized by large _______ due to a neural, neuropil, and synaptic loss
A
- Positive lesions (due to accumulation),
characterized by the
accumulation of neurofibrillary tangles,
amyloid plaques, dystrophic neurites, neuropil threads, and other deposits found in the brains - Negative lesions (due to losses), that are characterized by large atrophy due to a neural, neuropil, and synaptic loss
13
Q
Alzheimer’s Disease Pathophysiology:
- Widespread _____ of the cortex
- Neuritic plaques composed of extracellular
______ ______ _______ deposition - Neurofibrillary tangles composed of
________ ____ proteins - Common to see signs of vascular ______
damage and _________ ______
A
Alzheimer’s Disease Pathophysiology:
- Widespread atrophy of the cortex
- Neuritic plaques composed of extracellular
amyloid beta protein deposition - Neurofibrillary tangles composed of
hyperphosphorylated tau proteins - Common to see signs of vascular ischemic
damage and hippocampal sclerosis
14
Q
Alzheimer’s Disease:
Genetics:
1. All known mutations increase production of ____-______ proteins
2. ________ ____ patients – 3 copies of gene for
_______ precursor protein
3. Abnormality of gene controlling ___________
(cholesterol transporter) – accelerated deposition
of amyloid
4. Generation of anti-_______ ___________ in
Alzheimer disease appear to attenuate disease
process
A
Alzheimer’s Disease:
Genetics:
1. All known mutations increase production of beta-amyloid proteins
2. Trisomy 21 patients – 3 copies of gene for amyloid precursor protein
3. Abnormality of gene controlling apolipoprotein (cholesterol transporter) – accelerated deposition of amyloid
4. Generation of anti-amyloid antibodies in Alzheimer disease appear to attenuate disease process
15
Q
Risk factors for Alzheimer’s (6):
A
Several risk factors
* increasing age
* genetic factors
* head injuries
* vascular diseases
* Infections
* environmental factors -
heavy metals, trace
metals, and others
Cerebrovascular disease caused by hypertension &
atherosclerosis may play role in dementia
16
Q
_______, _________, & ________ increase risk
for developing dementia & progression of Alzheimer’s
A
Hypertension, diabetes, & hyperlipidemia increase risk for developing dementia & progression of Alzheimer’s
17
Q
T/F
Lifestyle factors do not directly affect Alzheimer’s
disease pathology but can still contribute to a negative
outcome in individuals with Alzheimer’s disease.
A
False
Lifestyle factors do not directly affect Alzheimer’s
disease pathology but can still contribute to a POSITIVE
outcome in individuals with Alzheimer’s disease.
18
Q
Promising pharmacological treatments for Alzheimer’s are poised at
advanced stages of clinical trials and include (3)
A
anti-amyloid β
anti-tau
anti-inflammatory strategies.
19
Q
Clinical Phases of Alzheimer’s:
- Pre-clinical or the pre-symptomatic stage:
- mild _______ loss
- early pathological changes in ______ and ________
- no functional impairment in _____
- absence of clinical signs and symptoms
A
Clinical Phases of Alzheimer’s:
- Pre-clinical or the pre-symptomatic stage:
- mild memory loss
- early pathological changes in cortex and hippocampus
- no functional impairment in ADLs
- absence of clinical signs and symptoms
20
Q
Clinical Phases of Alzheimer’s:
- Mild or early stage
* _______ start to appear in patients
* trouble in the daily life
* loss of ________ and _______
* disorientation of place and time
* change in _____
* development of ________
A
Clinical Phases of Alzheimer’s:
- Mild or early stage
* symptoms start to appear in patients
* trouble in the daily life
* loss of concentration and memory
* disorientation of place and time
* change in mood
* development of depression
21
Q
Clinical Phases of Alzheimer’s:
- Moderate stage
* disease spreads to _______ ______ areas
* increased memory loss
* trouble _________
* loss of ______ control
* difficulty in ______, ______, and ______
A
Clinical Phases of Alzheimer’s:
- Moderate stage
* disease spreads to cerebral cortex areas
* increased memory loss
* trouble recognizing family and friends
* loss of impulse control
* difficulty in reading, writing, and speaking
22
Q
Clinical Phases of Alzheimer’s:
- Severe AD or late-stage
* spread of the disease to the entire _____ area
* severe accumulation of _______ ______ and __________ tangles
* progressive functional and cognitive impairment - cannot recognize their family at all
* become ______
* difficulties in ______ and ______
* eventually leading to ____
A
Clinical Phases of Alzheimer’s:
- Severe AD or late-stage
* spread of the disease to the entire cortex area
* severe accumulation of neuritic plaques and neurofibrillary tangles
* progressive functional and cognitive impairment - cannot recognize their family at all
* become bedridden
* difficulties in swallowing and urination
* eventually leading to death
23
Q
Frontotemporal Dementia
Neurodegenerative disorder is a spectrum of clinical syndromes
characterized by ______ degeneration involving the ______ and
_____ ________ lobes of the brain
A
Frontotemporal Dementia
Neurodegenerative disorder is a spectrum of clinical syndromes
characterized by neuronal degeneration involving the frontal and
anterior temporal lobes of the brain
24
Q
Frontotemporal Dementia
Neurodegenerative disorde :
Clinical manifestations (5):
Etiology (2):
A
Clinical manifestations (5):
* behavior changes
* dietary changes
* loss of empathy
* Apathy
* Executive function
Etiology (2):
* Genetic
* Head trauma and thyroid disease linked with the development
25
Chronic Traumatic Encephalopathy
(CTE):
Neurodegenerative disease exhibiting a distinct pattern of neuropathological changes associated with _________ leading to increased risk of long-term memory and cognition issue.
Causes lesions at traumatic stress points leading to (3):
Chronic Traumatic Encephalopathy
(CTE):
Neurodegenerative disease exhibiting a distinct pattern of neuropathological changes associated with repetitive head trauma leading to increased risk of long-term memory and cognition issue.
Causes lesions at traumatic stress points leading to (3):
* axonal injury
* micro-hemorrhages
* subsequent loss of blood brain barrier integrity
26
Dementia Anesthesia Considerations:
Assessment of cognitive ability, capacity for decision making, & risk factors for POD
* Preoperative neuropsychiatric assessment –
establish baseline
Mini-Cog Assessment:
* Highly sensitive & specific for dementia
* Unbiased by variances in education & language
Criteria for Decision-making Capacity
1. Understanding treatment options
2. Appreciating & acknowledging medical condition & outcomes
3. Exhibiting reasoning & engaging in rational discussion of surgical treatment options
4. Clearly choosing a preferred treatment option
CNS changes result in increased sensitivity to anesthetic
agent
Changes in mood, memory, & motor function
* Increased risk for POD or further decrease in cognitive
disfunction
* Increased sensitivity d/t receptor downregulation
* Blood-brain barrier more permeable
* Decreased nerve conduction velocity
Pharmacological Interactions
Comprehensive medication list – multitude of anesthetic
implications
CNS changes result in increased sensitivity to anesthetic
agent
27
Frontotemporal Dementia
Neurodegenerative disorder:
Treatment (2 categories):
Frontotemporal Dementia
Neurodegenerative disorder:
Treatment (2 categories):
Non-pharmacologic:
social support services, physical therapy
& occupational therapy, speech therapy, cognitive behavior therapy, rehabilitation services, and caregivers' education
Pharmacologic:
* Acetylcholinesterase inhibitors and N-methyl-D-aspartate inhibitors
* Selective serotonin reuptake inhibitors (SSRIs)
* Antipsychotics
* Dopaminergic antagonists
* Salsalate (tau acetylation inhibitor) and gosuraneb (anti-tau monoclonal antibodies)
28
Frontotemporal Dementia
Neurodegenerative disorder
Pharmacologic Treatment:
Frontotemporal Dementia
Neurodegenerative disorder
Pharmacologic:
* Acetylcholinesterase inhibitors and N-methyl-D-aspartate inhibitors
* Selective serotonin reuptake inhibitors (SSRIs)
* Antipsychotics
* Dopaminergic antagonists
* Salsalate (tau acetylation inhibitor) and gosuraneb (anti-tau monoclonal antibodies)
29
Chronic Traumatic Encephalopathy
(CTE):
Trigger an ________ cascade and a deposition of:
phosphorylated tau (p-tau) protein amyloid-beta (Aβ)
TDP-43
neurofibrillary triangles
neutrophil neurites
astrocytic tangles
neuronal loss and cerebral atrophy with white matter changes.
Symptoms (7):
Chronic Traumatic Encephalopathy
(CTE):
Trigger an inflammatory cascade and a deposition of:
*phosphorylated tau (p-tau) protein *amyloid-beta (Aβ)
*TDP-43
*neurofibrillary triangles
*neutrophil neurites
*astrocytic tangles
*neuronal loss and cerebral atrophy with white matter changes.
Symptoms (7):
* changes in behavior
* cognition and motor symptoms
* impulsivity, paranoia, rage behaviors,
* headaches
* memory deficits, impaired attention
* dysphagia, dysarthria,
* coordination problems
30
* Most prevalent demyelinating disorders
* Combinations of inflammation, demyelination, and axonal
damage in the central nervous system
* Loss of myelin covering the axons is followed by formation of
demyelinated plaques.
* Immune mediated inflammatory disease
Multiple Sclerosis (MS)
31
Common demyelinating diseases that
affect your central nervous system
(brain and spinal cord) include (6):
* Multiple sclerosis (MS)
* Neuromyelitis optica spectrum disorder (NMOSD)
* Transverse myelitis (TM)
* Acute disseminated
encephalomyelitis (ADEM)
* Progressive multifocal
leukoencephalopathy (PML).
* Central pontine myelinolysis
(osmotic demyelination
syndrome).
32
Multiple Sclerosis (MS) attacks what anatomical structures (3):
* myelin
* oligodendrocytes (myelin producing cells)
* underlying nerve fibers
33
Multiple
Sclerosis (MS) Symptoms (11):
a) Fatigue
b) Tingling
c) Numbness
d) Muscle weakness
e) Ataxia
f) Vertigo
g) Tremor
h) Spasticity
i) Bowel & bladder disfunction
j) Pain
k) Heat intolerance
34
Multiple Sclerosis:
Contribute to ________ & _______
* Affects young adults between ages ___-___ years of age
* ______ affected two times more than ___
* Significant disability results in __ - __ years
* Characterized by periods of ______ & _______
Multiple Sclerosis:
Contribute to demyelination & neurodegeneration
* Affects young adults between ages 20-40 years of age
* Females affected two times more than males
* Significant disability in 20 -25 years
* Characterized by periods of relapse & remission
35
Multiple
Sclerosis (MS) Diagnosis (3):
a) MRI
b) Elevated IgG in the cerebrospinal fluid
c) Decreased conduction velocity on evoke potential studies
36
Treatment of Multiple
Sclerosis (MS):
__________ agents directed toward reducing
formation of new lesions & decreasing incidence of relapse
Treatment of Multiple
Sclerosis (MS):
Immunomodulatory agents directed toward reducing
formation of new lesions & decreasing incidence of relapse
37
Multiple Sclerosis (MS) Risk Factors (6):
Risk Factors:
a) female sex
b) exposure to Epstein-Barr or varicella zoster viruses
c) diabetes mellitus type 1
d) inflammatory bowel disease
e) low vitamin D levels
f) smoking
38
Multiple Sclerosis Anesthesia Considerations:
* Consider the impact of surgical ______ on the natural ______ of the disease
* Possible signs & symptoms of MS will be ______ _______
* infection and fever: increased body temperature results in complete _____ of _____ in __________ nerves
Multiple Sclerosis Anesthesia Considerations:
* Consider the impact of surgical stress on the natural progression of the disease
* Possible signs & symptoms of MS will be exacerbated postoperatively
* infection and fever: increased body temperature results in complete block of conduction in demyelinated nerves
39
Multiple Sclerosis Anesthesia Considerations:
T/F
There is NO evidence to support the use of one inhaled or injected anesthetic drug over another
Multiple Sclerosis Anesthesia Considerations:
TRUE
There is NO evidence to support the use of one inhaled or injected anesthetic drug over another
40
Multiple Sclerosis Anesthesia Considerations:
**Muscle relaxants**
* Avoid use of _______ in patients with _____ weakness
use of _______ can result in exaggerated ________ release and should be avoided
Multiple Sclerosis Anesthesia Considerations:
Avoid use of succinylcholine in patients with **motor** weakness
use of **succinylcholine** can result in exaggerated **potassium** release and should be avoided
41
Multiple Sclerosis Anesthesia Considerations:
**Muscle Relaxants**
* Avoid use of succinylcholine in patients with ______ weakness
* _______ responses to the paralyzing effects of _________ muscle relaxants
* coexisting skeletal muscle ______ and decreased skeletal muscle _____
* _______ to the effects of nondepolarizing muscle relaxants has been observed
* reflects the proliferation of extrajunctional ________ receptors characteristic of ______ motor neuron lesions
Multiple Sclerosis Anesthesia Considerations:
**Muscle Relaxants**
* Avoid use of succinylcholine in patients with motor weakness
* Prolonged responses to the paralyzing effects of nondepolarizing muscle relaxants
* coexisting skeletal muscle weakness and decreased skeletal muscle mass
* Resistance to the effects of nondepolarizing muscle relaxants has been observed
* reflects the proliferation of extrajunctional cholinergic receptors characteristic of upper motor neuron lesions
42
Multiple Sclerosis Anesthesia Considerations:
* Corticosteroid supplementation – consideration in patients on long-term corticosteroids
These patients are often on corticosteroid supplementation. Ask if taking corticosteroids, how much, when was last dose:
Chronic corticosteroid use can cause adrenal suppression, they are not producing sufficient quantities of endogenous hormones. Once patient is anesthetized the BP will bottom out.
Always give a dose prior to induction
43
Multiple Sclerosis Anesthesia Considerations:
Regional anesthetic techniques - changing and unpredictable neurologic presentation during the perioperative period must be appreciated
* hypothesized that intrathecal administration of _____ anesthetics promoted demyelination in the spinal cord
* ______ regions of the spinal cord may be _____ susceptible to the ______ effects of ______ anesthetics
* _____ and _____ analgesia & anesthesia have been used safely
Multiple Sclerosis Anesthesia Considerations:
Regional anesthetic techniques - changing and unpredictable neurologic presentation during the perioperative period must be appreciated
* hypothesized that intrathecal administration of local anesthetics promoted demyelination in the spinal cord
* Demyelinated regions of the spinal cord may be more susceptible to the neurotoxic effects of local anesthetics
* epidural and spinal analgesia & anesthesia have been used safely
44
GBS Progression:
________ response triggers an _________ response to peripheral nerves & spinal root
Symptoms progress over several days to reach peak at ___ to ___ weeks
* max loss of function ___ hours
* 4 weeks ______ _______ to limit of symptoms
* Recovery protracted for months to years – depend on extent of ______ injury
GBS Progression:
Autoimmune response triggers an autoimmune response to peripheral nerves & spinal root
Symptoms progress over several days to reach peak at 2 to 4 weeks
* max loss of function 72 hours
* 4 weeks most progressed to limit of symptoms
* Recovery protracted for months to years – depend on extent of nerve injury
45
Most common variant of GBS - Acute Inflammatory demyelinating polyneuropathy (AIDP)
Manifest as:
* _______ _______ muscle weakness that progressively leads to severe flaccid _____ &
respiratory _____
* Sensory & motor features depend on _____
* _____ of patients have history of ____ or _____ infection
* Severe limb weakness
* Related to ______ antibody response against GMI & GDI a gangliosides
MFS
* Anti-GQ1b antibodies
Most common variant of GBS - Acute Inflammatory demyelinating polyneuropathy (AIDP)
Manifest as:
* symmetric ascending muscle weakness that progressively leads to severe flaccid paralysis &
respiratory failure
* Sensory & motor features depend on subtype
* Half of patients have history of bacterial or viral infection
* Severe limb weakness
* Related to autoimmune antibody response against GMI & GDI a gangliosides
MFS
* Anti-GQ1b antibodies
* Symptoms affect cranial nerves resulting in clinical triad: ophthalmoplegia, ataxia, & areflexia
46
Common demyelinating diseases that
affect your peripheral nervous system
include (3):
* Guillain-Barré
syndrome (GBS)
* Charcot-Marie-Tooth
disease (CMT)
* Chronic inflammatory
demyelinating
polyneuropathy (CIDP)
47
Guillain-Barré
syndrome (GBS):
Occurring at a rate of 1-2 cases/100,000 persons per
year worldwide
* Increases with ____
* More prevalent in ___
Guillain-Barré
syndrome (GBS)
Occurring at a rate of 1-2 cases/100,000 persons per
year worldwide
* Increases with age
* More prevalent in men
48
Most common variant of GBS
Acute Inflammatory demyelinating polyneuropathy (AIDP)
49
GBS Symptoms:
affect ______ nerves resulting in clinical **triad**:
GBS Symptoms:
affect cranial nerves resulting in clinical triad:
*ophthalmoplegia
*ataxia
*areflexia
50
* Progressive dementia combined with choreoathetosis
* Marked atrophy of the caudate nucleus - lesser degree putamen & globus pallidus
* Abnormal movements caused by the loss of most of the cell bodies:
* GABA-secreting neurons in the caudate nucleus & putamen
* Acetylcholine-secreting neurons in many parts of the brain
* Loss of inhibition allows spontaneous outbursts of globus pallidus & substantia nigra activity that cause the
distortional movements
Treatment
* Supportive - directed at decreasing the choreiform movement
* Haloperidol and other butyrophenones - control the chorea and emotional lability
* Drugs that interfere with the neurotransmitter effects of dopamine
* antagonizing dopamine (risperidone, olanzapine)
* depleting dopamine stores (tetrabenazine, deutetrabenazine)
Anesthesia Considerations
* Preoperative sedation - butyrophenones such as droperidol or haloperidol - controlling choreiform movements
* Increased likelihood of pulmonary aspiration
* Acceptable anesthesia techniques include
* Nitrous oxide & inhalational anesthetics
* Propofol & succinylcholine
* Spinal anesthesia
?????
51
Stroke Risk factors (8):
* Hypertension
* Diabetes
* Smoking
* Atherosclerosis
Stroke-related disorders of the cerebrovascular system
* atherosclerotic disease of the carotid artery
* cerebral aneurysm
* arteriovenous malformation
* moyamoya disease.
52
Blood supply to the brain is via two pairs of vessels:
* internal carotid arteries
* vertebral arteries
53
Vessels join on the inferior surface of the brain to form the _____ of _____ - during ideal circumstances, provides collateral circulation to multiple areas of the brain.
Vessels join on the inferior surface of the brain to form the Circle of Willis - during ideal circumstances, provides collateral circulation to multiple areas of the brain.
54
Carotid arteries vessels comprise the ______ circulation (5):
Carotid arteries vessels comprise the anterior circulation (5):
* Frontal
* Parietal
* lateral temporal lobes
* basal ganglia
* most of the internal capsule
55
Vertebral arteries each give rise to a ______-______ cerebellar artery before converging at the level of the _____ to form the
_______ artery
Areas (5):
Vertebral arteries each give rise to a posterior-inferior cerebellar artery before converging at the level of the pons to form the
basilar artery
Areas (5):
* Brainstem
* occipital lobes
* Cerebellum
* medial portions of the temporal lobes
* most of the thalamus
56
Ischemic Stroke
Prognosis depends on the _____ _______ from the onset of symptoms to thrombolytic intervention if thrombosis is the cause
of the symptoms.
Ischemic Stroke
Prognosis depends on the time elapsed from the onset of symptoms to thrombolytic intervention if thrombosis is the cause
of the symptoms.
57
An ischemic stroke is the result of an _______ of a vessel that supplies a region of brain resulting in cellular ______ and subsequent
cellular ________.
An ischemic stroke is the result of an occlusion of a vessel that supplies a region of brain resulting in cellular ischemia and subsequent
cellular death.
58
Parkinson's Disease:
Nonmotor Features (4):
Parkinson's Disease:
Nonmotor Features:
1. sleep disturbances
2. depression and anxiety
3. autonomic dysfunction
4. cognitive impairment in advanced stages
59
Parkinson’s Disease – paralysis agitans:
Widespread degeneration of the portion of the _______ ______ that
sends _________ secreting nerve fibers to the _____ ______ and ________.
Parkinson’s Disease – paralysis agitans
Widespread degeneration of the portion of the substantia nigra that
sends dopamine secreting nerve fibers to the caudate nucleus and
putamen.
60
Parkinson's Disease:
_______ is presumed to inhibit the rate of firing of the neurons that control the _________ motor system.
Parkinson's Disease:
Dopamine is presumed to inhibit the rate of firing of the neurons that control the extrapyramidal motor system.
61
Parkinson's Disease:
1. Loss of ______ fibers normally present in
the ____ _______
2. Result regional _____ concentrations are
______
3. Depletion of ______ results in diminished
______ of these neurons and unopposed
stimulation by __________
Parkinson's Disease:
1. Loss of dopaminergic fibers normally present in
the basal ganglia
2. Result regional dopamine concentrations are
depleted
3. Depletion of dopamine results in diminished
inhibition of these neurons and unopposed
stimulation by acetylcholine
62
Parkinson’s Disease – paralysis agitans:
Symptoms:
* ______ of much of the _______ of the body
* Involuntary _____ at a fixed rate of 3 to 6 cycles/sec of the involved areas (resting)
* Serious difficulty in initiating movement, called –
______
* Postural instability caused by impaired _____
reflexes, leading to poor balance and falls
* Other motor symptoms, including ______
(impaired ability to swallow), _____ disorders,
____ disturbances, and ______
Parkinson’s Disease – paralysis agitans:
Symptoms:
* Rigidity of much of the musculature of the body
* Involuntary tremor at a fixed rate of 3 to 6
cycles/sec of the involved areas (resting)
* Serious difficulty in initiating movement, called –
akinesia
* Postural instability caused by impaired postural
reflexes, leading to poor balance and falls
* Other motor symptoms, including dysphagia
(impaired ability to swallow), speech disorders,
gait disturbances, and fatigue
63
Parkinson's Disease:
Rigidity: destruction of the _______ neurons in the _____ ______ allow the caudate nucleus and putamen to
become overly active and possibly cause continuous output of _______ signals to the ________ motor control system
Parkinson's Disease:
Rigidity: destruction of the dopaminergic neurons in the substantia nigra allow the caudate nucleus and putamen to
become overly active and possibly cause continuous output of
excitatory signals to the corticospinal motor control system
64
Parkinson's Disease:
Involuntary Tremor:
feedback circuits ______ because of high
feedback gains after loss of their inhibition (occurs during all ______ hours)
Parkinson's Disease:
Involuntary Tremor:
feedback circuits oscillate because of high feedback gains after loss of their inhibition (occurs during all waking hours)
65
Parkinson's Disease:
Akinesia - dopamine secretion in the _____ system (nucleus accumbens) is decreased, along with its decrease in the basal ganglia - this decrease might reduce the _____ for motor
activity so greatly that akinesia results
Parkinson's Disease:
Akinesia - dopamine secretion in the limbic system (nucleus accumbens) is decreased, along with its decrease in the basal ganglia - this decrease might reduce the psychic drive for motor
activity so greatly that akinesia results
66
Parkinson's Treatment:
Goal of therapy: increase concentrations of ______ in the basal ganglia or
decrease the neuronal effects of ____________
Parkinson's Treatment:
Goal of therapy: increase concentrations of dopamine in the basal ganglia or
decrease the neuronal effects of acetylcholine
67
Parkinson's Treatments:
1. Levodopa
* Dopamine precursor
* converted into dopamine (brain) - restores the normal balance between inhibition and excitation in the caudate nucleus and putamen
* ameliorates many of the motor disturbances, especially the rigidity and akinesia
* little beneficial effect on nonmotor symptoms
Monoamine oxidase inhibitors
* monoamine oxidase is responsible for destruction of most of the dopamine after it has been secreted
* any dopamine that is released remains in the basal ganglial tissues for a longer time
* helps to slow destruction of the dopamine-secreting neurons in the substantia nigra
2. Transplanted Fetal Dopamine Cells:
* Transplantation into the caudate nuclei and putamen has been used with some short-term success to treat Parkinson’s disease
3. Surgical treatment:
* Ablative treatments – pallidotomy & thalamotomy
* Implantations deep brain stimulating device
* Transcranial magnetic resonance-guided focus ultrasound
68
Huntington’s Disease:
___________ ________ hereditary disease – trinucleotide repeats in the gene for Huntington’s
Huntington’s Disease:
Autosomal dominant hereditary disease – trinucleotide repeats in the gene for Huntington’s
69
________ is characterized by sudden neurologic deficits
resulting from ischemia (____% of cases) or hemorrhage
(____% of cases).
Stroke is characterized by sudden neurologic deficits
resulting from ischemia (88% of cases) or hemorrhage
(12% of cases).
70
The anterior and posterior circulations communicate via the _______
communicating artery, and the left and right ______ cerebral arteries
communicate via the _______ communicating artery.
The anterior and posterior circulations communicate via the posterior communicating artery, and the left and right anterior cerebral arteries
communicate via the anterior communicating artery.
Occlusion of specific arteries distal to the Circle of Willis results in
predictable clinical neurologic deficits.
71
T/F
Occlusion of specific arteries distal to the Circle of Willis results in predictable clinical neurologic deficits.
TRUE
72
A transient ischemic attack (TIA) is a _____ vascular-related focal neurologic deficit that resolves
within ___ hours without intervention.
*~ ____-______ of patients who suffer a TIA will suffer
a stroke
A transient ischemic attack (TIA) is a sudden vascular-related focal neurologic deficit that resolves
within 24 hours without intervention.
*~ 1/3 of patients who suffer a TIA will suffer
a stroke
73
Risk of acute ischemic stroke (6):
* Systemic hypertension - most significant risk factor
* Cigarette smoking
* Hyperlipidemia
* Diabetes mellitus
* Excessive alcohol consumption
* Increased serum homocysteine
concentrations
74
Stroke Anesthesia Considerations:
Pre-operative considerations:
* _____ is important – event to intervention is crucial (rapid)
* Depressed _____
* Ability to protect
_____
* Claustrophobic
* Anxiety
* Full stomach/ GERD
* Pulmonary disorders
* _______ status
* Impact choice of
_______ medications &
________ goals
Stroke Anesthesia Considerations:
Pre-operative considerations
* Time is important – event to intervention is crucial (rapid)
* Depressed LOC
* Ability to protect
airway
* Claustrophobic
* Anxiety
* Full stomach/ GERD
* Pulmonary disorders
*Neurological
status
* Impact choice of
vasoactive medications &
hemodynamic goals
75
Stroke Anesthesia Considerations:
Maintain PaO2:
* Above ____ mmHG
* SaO2 above ___%
Maintain BP
Before revascularization:
* Systolic -____ to ____ mmHg
* Diastolic – below ___ mmHg
After
revascularization
* Systolic ____ – ____ mmHg
Fluids
* ______
* ______
* Avoid fluids containing ____
Glucose Level
* Between ____ -_____
mg/dL
* Below ___ mg/dL –
treat w/dextrose solution
Heparin
* ACT of _____ – ____seconds
* _______ reversal (give
slowly)
Stroke Anesthesia Considerations:
Maintain PaO2
* Above 60 mmHG
* SaO2 above 92%
Maintain BP
Before revascularization
* Systolic 140-180 mmHg
* Diastolic – below 105 mmHg
After
revascularization
* Systolic -120 –140 mmHg
Fluids:
* Isotonic
* Euvolemia
* Avoid fluids
containing glucose
Glucose Level:
* Between 140 -180 mg/dL
* Below 60 mg/dL – treat w/dextrose solution
Heparin:
* ACT of 250 – 300
seconds
* Protamine
reversal (give
slowly)
76
Intraparenchymal Hemorrhage:
bleeding that occurs within the brain's functional tissue, or parenchyma
77
Extradural Hemorrhage:
Involve arteries that supply the _____ _____ located
between the ____ _____ & ______ of the cranial
bones – accumulation of blood in ______ space
Compress the brain & decrease perfusion
Extradural Hemorrhage:
Involve arteries that supply the dura mater located
between the dura mater & periosteum of the cranial
bones – accumulation of blood in epidural space
Compress the brain & decrease perfusion
78
Subdural Hemorrhage:
Blood accumulation between ____ _____ & ______ layer - Rupture of bridging veins that run in the _____ space
Subdural Hemorrhage:
Blood accumulation between dura mater & arachnoid layer - Rupture of bridging veins that run in the subdural space
79
Cerebral aneurysm are abnormal, localized ______ of the intracranial arteries
Cerebral aneurysm are abnormal, localized dilations of the intracranial arteries
Classifications
* Berry
* Mycotic
* Traumatic
* Fusiform
* Neoplastic
* Atherosclerotic
80
An estimated __ million people in the US have an
unruptured cerebral aneurysm.
Ruptured aneurysms are fatal in approximately ___%
cases
Giant aneurysm – greater than ___ inch in diameter
An estimated 6 million people in the US have an
unruptured cerebral aneurysm.
Ruptured aneurysms are fatal in approximately 40%
cases
Giant aneurysm – greater than 1 inch in diameter
81
Subarachnoid hemorrhage
Signs & Symptoms (7):
Subarachnoid hemorrhage
Signs & Symptoms (7):
* Intense headache
* Transient loss of consciousness
* Nausea & vomiting
* Photophobia
* Fever
* Meningism
* Focal neurological deficits
82
Vasospasm – delayed & sustained ________ cerebral arteries
* Leading cause morbidity & mortality with SAH after
aneurysm rupture
* Decrease in _____ ______ & ___
* Neurological deterioration arising from impaired ______ perfusion, ______, and secondary _______ of the brain peaks between the ____ and ____ day.
Vasospasm – delayed & sustained contraction cerebral arteries
* Leading cause morbidity & mortality with SAH after
aneurysm rupture
* Decrease in blood flow & CPP
* Neurological deterioration arising from impaired cerebral perfusion, ischemia, and secondary infarction of the brain
peaks between the 3rd and 14th day.
83
Cerebral Vasospasm Treatment:
* Oral nimodipine & hypertensive therapy
* Ballon angioplasty & intraarterial vasodilator infusion
* Papaverine - Off-label use calcium channel antagonist
Prevent & Treat Ischemic Neurological Deficits:
* Hypervolemia – colloids & crystalloids
* Hypertension – fluid loading & vasopressors
* Hemodilution – 27% - 30%
Maintain systolic BP
* 120 – 150 mmHg before clipping
* Max 160 -180 mmHg systolic & MAP 110 mmHg after clipping
Maintain HR
80 – 120 b/min
Management of intracranial aneurysm rupture (Box 31.8
Nagelhout: page 737)
84
Intracranial
Space:
* Total volume of contents -1300 to 1500ml
* Components
* Brain (80% to 90% of volume)
* Blood
* Intracellular water
* Cerebral Spinal Fluid (CSF)
* Brain is not compressible, any increase in total intracranial volume produces an
accompany increase in ICP
* Any expansion of one component
necessitates a reduction of another component if ICP is to remain constant.
CSF is absorbed
* microscopic arachnoid villa
* macroscopic arachnoid granulations
* dura matter
* bordering venous sinusoids
* sinuses
* blood-brain barrier
85
Cerebrospinal Fluid
System:
Origin of secretions
* Choroid plexus in 4 ventricles
* Ependymal surfaces
Rate – 30ml/hr
* Entire CSF volume replaced every 3 to 4 hours
Absorption
* Arachnoid villi act as valves
86
Monro-Kellie Doctrine:
The cranium (or neurocranium) describes the part of the skull
encasing the brain, made up of 8 bones (frontal, ethmoid, sphenoid,
occipital, paired parietals, and paired temporal). As the cranium is
made from solid bone*, its structure is fixed and therefore the volume
contained within cannot be changed.
The intracranial pressure (ICP) is the pressure within the cranium
of the skull. Due to the fixed nature of the cranium, an increase in
volume of any one of the intracranial components will also cause an
increase in pressure.
Therefore, in the absence of pathology, an equilibrium between
these three components must be maintained to preserve a normal
intracranial pressure. If the volume of one of the components
within the cranium increases, the volume of a different component
must decrease to maintain this equilibrium and sustain a normal ICP.
87
Intracranial:
Various meningeal barriers within the intracranial vault that functionally separate
the contents:
Falx cerebri (a reflection of dura mater that separates the two cerebral
hemispheres)
Tentorium cerebelli (a reflection of dura mater that lies rostral to the cerebellum and marks the border between the supratentorial and infratentorial spaces).
Intracranial Vault
If one of the other components increases in size or a new
component (with its own volume and own contribution to intracranial
pressure) is introduced into the cranial cavity, its volume may be small enough that the skull volume can accommodate and
compensatory mechanisms can be employed to maintain a normal
intracranial pressure.
The main compensatory mechanisms are increased drainage of blood or cerebrospinal fluid from the cranial cavity.
Once volume compensation has reached exhaustion, the
subsequent increasing ICP has a direct relationship with a reduction in cerebral perfusion and an increased risk of herniation.
88
Subfalcine herniation -
herniation of cerebral
hemispheric contents
under the falx cerebri
Leads to compression of branches of the anterior
cerebral artery and is evident on radiographic imaging
as midline shift
Transtentorial herniation
- brainstem compression
occurs in a rostral to
caudal manner
altered consciousness, defects in gaze and afferent ocular reflexes, and, finally, hemodynamic and respiratory compromise followed by death
Uncal herniation - uncus
(i.e., the medial portion of
the temporal lobe)
herniate over the
tentorium cerebelli
* ipsilateral oculomotor nerve dysfunction because the
oculomotor nerve is compressed against the brainstem
* pupillary dilatation, ptosis, and lateral deviation of the
affected eye, which occurs before evidence of
brainstem compression and death.
89
Intracranial Pressure (ICP):
* Supratentorial cerebral spinal fluid pressure
* Normal ICP 5 to 15 mmHg
(adults)
* Intracranial hypertension:
20 to 25 mmHg
* Cerebral Spinal Fluid (CSF)
produced at a constant rate of 500 to 600 ml/day
90
Increased ICP Signs & Symptoms:
* Papilledema
* Unilateral or bilateral mydriasis
* Headache – postural, worse in the morning, made worse by coughing
* Nausea & Vomiting
* Slurred speech
* Disoriented & altered levels of consciousness
* Flaccid hemiplegia or hemiparesis
* Abduction or oculomotor palsy
* Neck rigidity
* Respiratory disturbances
* Arterial hypertension, w/bradycardia
* Appearance of Q wave, deep & inverted T-waves, prolonged OT intervals, & ST segment elevation
91
Causes of Increased ICP (5):
*Aqueductal stenosis
*Benign intracranial hypertension
*Normal pressure hydrocephalus
*Intracranial Hemorrhage
*IIntracranial tumors
92
Stenosis of major CSF flow channels:
* impede CSF flow
* lead to increased ICP
Common causes of obstructive hydrocephalus - congenital narrowing of the cerebral aqueduct that connects the third and fourth ventricles
* Characterized by ICP higher than 20 mm Hg, normal CSF composition, normal sensorium,
and absence of local intracranial lesions.
* Obese women
* Patients with various systemic diseases, including polycystic ovary syndrome, systemic lupus erythematosus, Addison disease, hypoparathyroidism, and hypervitaminosis A
* Triad of dementia, gait changes, and urinary incontinence – develops over a period of
weeks to months
* Related to compensated but impaired CSF absorption from a previous insult
(subarachnoid hemorrhage, meningitis, or head trauma)
* Lumbar puncture usually reveals normal or low CSF pressure, yet CT or MRI will often demonstrate large ventricles
93
Highly invasive (strict sterile technique required)
* Allows drainage of CSF to lower ICP
Gold Standard – Intraventricular catheter
* CSF leak
* Systemic infection
* Prophylactic antibiotics nor routine catheter exchange do NOT decrease incidence of infection
* Intraventricular hemorrhage
* Craniotomy
Risk Factors
* Severe TBI
* Glasgow Coma Scale score less than 9 w/abnormal CT scan
* Normal CT scan w/ two or more;
* Age older than 40
* Unilateral or bilateral motor posturing
* Systolic blood pressure less than 90 mmHg
Recommended
94
Hydrocephalus: Excess water on the brain
* Communicating Hydrocephalus
* Caused by blockage of fluid flow in the subarachnoid spaces
around the basal region of the brain or blockage of the
arachnoid villa where fluid id
absorbed
* Non-communicating
Hydrocephalus
* Caused by a block in the
aqueduct of Sylvius, resulting from atresia (closure) before birth in many babies or from
blockage by a brain tumor at
any age
Treatment usually involves placement of a silicone tube from one of the ventricles to the peritoneal cavity.
95
Therapeutic Modalities:
Patent airway, Adequate ventilation, & Controlled ventilation
Surgical Decompression
* Hematoma, contusion, tumor, hygroma, hydrocephalus,
pneumocephalus
Hyperventilation
* Hypocapnia – reduced ICP reflex vasoconstriction
* Vasoconstriction
* Lower PaCO2 Respiratory alkalosis vasoconstriction
* CBF decreases by 4% per 1 mmHg decrease in PaCO2
* Not used 1st 24 hours in TBI patients
* Caution ischemia secondary to insufficient CBF (goal PaCO2 ~30 –
35 mmHg)
CSF Drainage
* Total volume 150 ml
* Secreted ependymal cells of choroid plexus – rate 30ml/hr
* Entire CSF volume replaced every 3 to 4 hours
* Cycled in 10-minute intervals
* Chronic – ventriculoperitoneal shunts
96
Hypothermia
* Management intractable intracranial hypertension
* Trauma or hemorrhage – bladder temp 35 C to 36 C for 48 hours
* Decrease CMRO2 by 7% for each degree centigrade decrease in core temp
* Pharmacologic
* Diuretics
1. Loop diuretics – general diuresis - furosemide, bumetanide, ethacrynic acid
2. Osmotic diuretics – decrease water content of brain – mannitol
1. 0.25 – 1 g/kg
2. Transient vasodilation – increase CBF – increase ICP
3. Begin 30 minutes, maximum effect 1 to 2 hours, & last up to 6 hours
3. Hypertonic saline – ICP reduction decrease water content (intact BBB) – 3% to
23.4%
* Osmotic effect on brain
* Rapid rise in serum sodium concentration greater than 9 mEq/L in 24 hours osmotic demyelination syndrome
* Reduction seen for ~ 2 hours
* Target goal: sodium 145 – 155 mEq/L & osmolarity 320 mOsm/L
* Corticosteroids
* Glucocorticoids – penetrate BBB & decrease edema associated with mass
lesions
* Barbiturates
* Barbiturate coma
Reduce refractory ICP – decreasing CMRO2 , scavenging free radicals,
preventing convulsions, & reducing hyperthermic response to ischemia
97
Increased ICP Anesthetic Considerations:
Avoid sedatives
* Extremely sensitive to the CNS-depressant effects of medications
(opioid)
* Consider serum concentrations of
anticonvulsant medication
* Continue corticosteroid therapy
* Monitor for hyperglycemia & treat
* Elevate head of bed 15 to 30 degrees during transport
* Judicious fluid management
* Avoid perioperative & postoperative hypertension
* Monitor for venous air embolus
* Induction slow & deliberate to avoid
change in ICP & CPP
* Slow & gentle emergence from anesthesia (avoid coughing & bucking)
98
Temporary disruptions of brain function caused by
uncontrolled excessive neuronal activity
Temporary symptomatic seizures
* Causes: multiple neurological or medical conditions
* Acute electrolyte disorders
* Hypoglycemia
* Drugs (e.g., cocaine)
* Eclampsia
* Kidney failure
* Hypertensive encephalopathy
* Meningitis Epilepsy
* Chronic condition of recurrent seizures - vary from brief and nearly undetectable symptoms to periods of vigorous shaking and convulsions
* Not a single disease
* Multiple underlying pathophysiological mechanisms that
cause cerebral dysfunction and injury
99
Epileptic Seizure Cause
* Disruption of the normal balance between inhibitory and excitatory currents or transmission in one or more regions of the brain
Classification
* Focal
* Generalized
Aura
Postictal period
* time after the seizure, prior to the return of normal neurological function
Post-seizure depression
* person remains in stupor for 1 minute to many minutes after the seizure attack is over and then often remains severely
fatigued and asleep for hours thereafter
100
Focal
Limited to a focal area of one cerebral hemisphere -
localized organic lesion or functional abnormality:
* scar tissue in the brain that pulls
on the adjacent neuronal tissue
* tumor that compresses an area of the brain
* destroyed area of brain tissue
* congenitally deranged local circuitry
Lesions can promote extremely rapid
discharges in the local neurons
* Classification
* Simple partial seizures
* no major change in consciousness
* confined to a single area of the brain
* Complex partial seizures
* consciousness is impaired
* repetitive movements
(automatisms), such as chewing or lip smacking
Types:
* Automatisms
* Behavior arrest
* Hyperkinetic
* Autonomic
* Cognitive
* Emotional
101
Generalized
Previously called grand mal seizures
Diffusely involve both hemispheres of the cerebral cortex
Abrupt loss of consciousness and extreme neuronal discharges in all areas of the brain
* the cerebral cortex, the deeper parts of the cerebrum, and even the brain stem
Types
* Motor - (tonic-clonic, clonic, tonic, myoclonic, myoclonic-tonic-clonic, myoclonic-atonic, atonic, epileptic spasms)
* Non-motor/absence - (typical, atypical, myoclonic, eyelid myoclonia)
Tonic-clonic seizures
* discharges transmitted all the way into the spinal cord sometimes cause generalized tonic seizures of the entire body, followed toward the end by alternating tonic and spasmodic muscle contractions
* majority of generalized seizures are idiopathic
* a hereditary predisposition
Absence seizures (petit mal seizures)
* usually begin in childhood or early adolescence
* involve the thalamocortical brain activating system person often stares and has twitchlike contractions of
muscles, usually in the head region, especially blinking of the eyes
* characterized by 3 to 30 seconds of unconsciousness or diminished consciousness
102
Seizure Treatment:
Antiepileptic drugs
* Blockade of voltage-dependent sodium channels (e.g., carbamazepine
and phenytoin)
* Altered calcium currents (e.g., ethosuximide
* Increase in GABA activity (e.g., phenobarbital and benzodiazepines)
* Inhibition of receptors for glutamate, the most prevalent excitatory
neurotransmitter (e.g., perampanel)
* Multiple mechanisms of action (e.g., valproate and topiramate, which
block voltage-dependent sodium channels and increase GABA levels
in the brain
Surgical excision of the focus
* EEG & MRI used to localize abnormal spiking waves originating in areas of organic brain disease that predispose to focal epileptic
attacks
* Resection of a pathologic region - a tumor, hamartoma, or scar tissue
* Corpus callosotomy may help to prevent the generalization of partial
seizures to the opposite hemisphere (rarely performed)
* Hemispherectomy is sometimes needed for persistent catastrophic
seizures (rarely performed)
103
Anesthesia Considerations
Pre-operative
* Focus on cause & type of seizure
* Medication regimen & last dose
* Last known episode
Perioperative
* Avoid metabolic abnormalities
* Aware of drug toxicities & adverse side effects
* Maintain antiseizure medication
* Avoid drugs with epileptogenic potential
* Ketamine & methohexital
Post-operative
* Observe for 4 – 6 hours after procedure
Perioperative Treatment
* Maintain or establish patent airway
* IV medications
* Propofol 50-100mg
* Phenytoin 500- 1000 mg slowly
* Benzodiazepine
* Diazepam 5-10 mg
* Midazolam 1-5 mg
* Correct metabolic abnormalities
104
Intracranial tumors may be classified as primary (those arising from the brain and its coverings) or metastatic.
Primary brain tumors (gliomas) - originate from virtually any cell type within the central nervous system
Classification depends on histologic cell type
Supratentorial tumors - more common in adults
* headache, seizures, or new neurologic deficits
Infratentorial tumors - more common in children
* obstructive hydrocephalus and ataxia
Treatment - surgical resection or debulking, chemotherapy, or radiation
As the tumor continues to grow, it will reach a certain size where these compensatory mechanisms will become exhausted
* no further drainage of blood or CSF possible
* equilibrium becomes disrupted
* patient enters a decompensated state
* intracranial pressure will begin to rise
Once volume compensation has reached exhaustion, the subsequent increasing ICP has a direct relationship
with a reduction in cerebral perfusion and an increased risk of herniation
105
Gliomas Astrocytes
* most prevalent glial cells
* give rise to many infratentorial &
supratentorial tumors
Gliomas are primary central nervous system tumors that arise from glial progenitor cells.
The annual incidence of gliomas is reported
to be about 6 cases per 100,000 worldwide.
Type of gliomas:
* Astrocytoma
* Oligodendroglioma
* Glioblastoma
Different genomic signatures lead to
different clinical outcomes, thus necessitating different expectations and
treatment methods
Low-grade gliomas –well-differentiated, less
aggressive
The annual incidence of gliomas is reported
to be about 6 cases per 100,000 worldwide.
106
Gliomas present with various symptoms, related to the location and
grade of the tumor.
Low-grade, slow-growing tumors
* present with new-onset seizure or a more subtle progressive neurologic deficit
Higher-grade, faster-growing tumors
* present with more acute neurologic symptoms combined with
other symptoms
Common presenting symptoms
* Headache
* Seizure
* Cognitive dysfunction
* focal neurologic deficits
Headache is one of the most common non-specific symptoms in patients with brain tumors; however, it has a very low positive
predictive value
107
Astrocytoma
Astrocytic tumors typically show diffusely infiltrating fibrillary glial cells with a microcytic background
and regional heterogeneity.
108
Oligodendroglioma
* Oligodendroglioma is a relatively slow-growing tumor with a predilection for the frontal lobe and is often associated with seizures.
* Common histopathologic findings include a “fried egg” appearance with uniformly rounded nuclei and clear halos, “chicken-wire” patterned branching capillaries, and extensive
calcifications.
*Generally associated with a favorable prognosis and a good response to chemotherapy.
109
Glioblastoma
* Glioblastoma is a highly malignant tumor that
occurs most commonly in elderly patients, accounting for around 49% of primary malignant brain tumor.
* The histologic hallmark of glioblastoma is necrosis and vascular proliferation, commonly seen together with marked pleomorphism and increased mitotic activity.
* Characterized by rapid progression and has a
median survival of 14–16 months after
diagnosis
110
Pituitary Tumor
10% intracranial neoplasms
Rarely metastatic
Hypersecretion of pituitary hormones
Symptoms
* Frontotemporal headache
* Bitemporal hemianopsia
* Excessive growth hormone
* Increased skeletal size
* Face, hands, & feet
* Intubation difficulty
* Coronary artery disease
* Hypertension
* Cardiomyopathy
* Hyperglycemia
111
Cerebral Palsy:
Most prevalent cause of persistent motor impairment in children –
affecting 1-2 / 1000 births in developed countries
Cause
* Antenatal or perinatal injury to developing brain
Characterizations
* Nonprogressive abnormal movement & posture
* Spasticity
* Ataxia
* Dyskinesias
* Mild to moderate
* Isolated or involve cognitive impairment, speech disorders, &
seizures
Require multiple orthopedic surgeries:
* Soft tissue release
* Tendon lengthening for contractures
* Osteotomies for hip deformities
* Pinal fusion for scoliosis
112
Cerebral Palsy:
Require psychosocial aspects as well as medical aspects of their
condition
Communications – cognitive delay, speech impairment, &
behavioral problems
* Special accommodations
* Parent or caretaker involvement
* Speech impairment does not imply cognitive impairment
Seizure involvement
* Antiepileptic medications – type & frequency
* Semiology
Gastrointestinal (risk of aspiration)
* GERD – common
* Bulbar involvement - chronic aspiration & feeding
difficulties – gastrostomy tube placement
Respiratory
* Infections
* Restrictive deficits – kyphoscoliosis – significant
pulmonary mobility impairment
Airway management
* Cervical kyphosis or dystonia
* Lower minimum alveolar concentration
* Prone to intraoperative hypothermia due to hypothalamic
dysfunction
* Correlation between cerebral palsy and latex allergy (exposure
to multiple surgical procedures
113
Spina Bifida:
Diverse group of congenital malformations of the spine & spinal cord
Pathophysiology
* Embryologically – failure of fusion of the neural tube
Open defects w/exposure of neural tissue
* Myelomeningocele & myeloschisis
* Associated w/ neurological deficits –repaired prenatally
Closed defects w/ skin covering
* Meningocele, tethered cord, & split cord
* Associated deficits vary – asymptomatic, sacral
dimple, hemangioma, or tuff of hair
Neurological Abnormalities
* Motor & sensory deficits below level of defect
* Chiari II malformations, hydrocephalus,
neurogenic bladder
114
Spina Bifida:
Surgical procedures
* Orthopedic
* Correction of congenital or acquired limb deformities (club foot, hip dislocation)
* Spinal fusion for scoliosis
* Release of contractures
* Tethered cord syndrome – cord release
Anesthesia implications
Neuraxial anesthesia
* Increased dura puncture & failed block due to whether
undergone corrective spinal surgery, anatomical abnormality
* ligamentum flavum may be malformed or absent
* Epidural space may be malformed or nonexistent
* Cord tethering can result in low termination of spinal
cord
* If necessary thorough understanding of patient’s anatomy is required
* MRI – allow examination of bony and ligamentous
defect, termination of spinal cord, & presence of
masses (lipoma & syrinx)
* Avoid needle placement through surgical scars
* Epidural placed above level of defect
* Smaller boluses
* Failed or incomplete block possible
115
Depression & Manic-Depressive Psychosis
Cause
* Presumption manifestations are caused by:
* brain deficiency in dopamine, norepinephrine, & serotonin
* Altered receptor activity
* norepinephrine-secreting neurons - located in the brain stem
* neurons send fibers upward to most parts of the brain limbic system, thalamus, and cerebral cortex
* serotonin-producing neurons - located in the midline raphe nuclei of the lower pons and medulla
* send fibers to many areas of the limbic system and to some other areas of the brain
Characterized
* Sadness & pessimism
* grief, unhappiness, despair, and misery
* lose their appetite and sex drive
* severe insomnia
116
1. Monoamine oxidase inhibitors
* Block destruction of norepinephrine and serotonin once they are formed
* Side effects
* Hypotension
* Agitation
* Muscle spasm
* Urinary retention
* Paresthesia
* Jaundice
* Use opioids with caution
* Avoid meperidine – hyperthermia, seizure, & coma
* Enhanced sympathetic activity with ketamine, pancuronium, &
epinephrine
2. Tricyclic Antidepressants
* Block reuptake of norepinephrine and serotonin by nerve endings
* Increased anesthetic requirements – enhanced brain catecholamine
activity
* Potentiation of centrally acting anticholinergic agents (atropine &
scopolamine)
* Increased likelihood of confusion & delirium
* Exaggerated response to indirect-acting vasopressors & sympathetic
stimulation
* Chronic therapy – depletion of cardiac catecholamines
Treatment
70% of depressive patients can be
treated effectively with drugs that
increase the excitatory effects of
norepinephrine and serotonin at the
nerve endings
3. Selective Serotonin Reuptake Inhibitors
* No anticholinergic activity
* Generally, do not affect cardiac conduction
* Serotonin Syndrome
* Agitation, hypertension, hyperthermia, tremor, acidosis, &
autonomic instability
4. Norepinephrine Dopamine Reuptake Inhibitor
117
Schizophrenia
Schizophrenia interferes with a person’s ability to think clearly, manage emotions, make decisions,
and relate to others.
Pathophysiology:
1. Multiple areas in the cerebral cortex prefrontal lobes
1. neural signals have become blocked
2. processing of the signals becomes dysfunctional b/c many synapses normally excited by the neurotransmitter glutamate
lose their responsiveness to this transmitter
2. Excessive excitement of a group of neurons that secrete dopamine in the behavioral centers of the
brain, including in the frontal lobes
3. Abnormal function of a crucial part of the brain’s limbic behavioral control system centered around the
hippocampus
4. Excessive dopamine
1. Excess dopamine is secreted by a group of dopamine-secreting neurons whose cell bodies lie in the ventral tegmentum
of the mesencephalon, medial and superior to the substantia nigra
2. Many drugs that are effective in treating schizophrenia, such as chlorpromazine, haloperidol, and thiothixene, all either
decrease secretion of dopamine at dopaminergic nerve endings or decrease the effect of dopamine on neurons
Characterizations
* Hearing voices and has delusions
* Intense fear
* Highly paranoid
* Develop incoherent speech
* Dissociation of ideas
* Abnormal sequences of thought
* Withdrawn & catatonic behavior
* Abnormal posture and even rigidity.
Schizophrenia: What It Is, Causes, Symptoms & Treatment
Risk Factors (No confirmed causes of schizophrenia)
* Environment
* Cerebral infections & autoimmune diseases
118
Stroke Etiologies (5):
* 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
119
Stroke Diagnosis (3):
* CT (non-contrast) - reliably
distinguishes acute
intracerebral hemorrhage from ischemia
* Conventional angiography -useful for demonstrating
arterial occlusion
* Transcranial Doppler
ultrasonography - indirect
evidence of major vascular
occlusion & real-time bedside monitoring in patients undergoing thrombolytic
therapy
120
Stroke Intervention Goal:
Goal: Restoring blood flow to ischemic penumbra & avoiding secondary cerebral damage
121
Stroke considerations:
Anesthetic technique based on _________
basis - multiple prospective studies did not
demonstrate increased risk or poor outcome in
those who received general anesthesia over
monitored anesthesia care
Stroke considerations:
Anesthetic technique based on individualized
basis - multiple prospective studies did not
demonstrate increased risk or poor outcome in
those who received general anesthesia over
monitored anesthesia care
122
Extradural Hemorrhage Symptoms:
*Progressive alteration in _____
* Increased ____
* Decreased ____
Treatment:
* Excellent prognosis with early ________ evacuation
Extradural Hemorrhage Symptoms:
*Progressive alteration in consciousness
* Increased ICP
* Decreased CPP
Treatment
* Excellent prognosis with early hematoma
evacuation
123
Subdural Hemorrhage:
Etiology (2):
Signs & symptoms (5):
Subdural Hemorrhage:
Etiology:
* Trauma
* Anticoagulant therapy
Signs & symptoms:
* Drowsiness
* Obtundation
* Hemiparesis
* Hemianopsia
* Language disturbances
124
Subdural Hemorrhage Treatment (4):
Treatment:
* Conservative medical stabilized condition
* Evacuation of hematoma
* Drained via Burr holes
* Craniotomy
125
Arteriovenous
Malformation:
Congenital intracerebral networks – ______ flow directly into _____
*Lack ability to ________
Arteriovenous
Malformation:
Congenital intracerebral networks – arteries flow directly into veins
*Lack ability to autoregulate
126
Arteriovenous
Malformation:
Signs & Symptoms (5):
Diagnosis (1):
Arteriovenous
Malformation
Signs & Symptoms:
* Headache
* New focal neurologic deficits
* Acute hemorrhage
* Seizures
* Hydrocephalus or macrocephaly
Diagnosis - MRI
127
Severity of a subarachnoid hemorrhage (SAH) can be graded clinically with either the _____ & _____ or World Federation Surgeons Scale (Nagelhout; page 734)
Severity of a subarachnoid hemorrhage (SAH) can be graded clinically with either the Hunt & Hess or World Federation Surgeons Scale (Nagelhout; page 734)
128
Despite maximal medical measures, ____% of patients who initially survive an SAH experience stroke or death secondary
to __________.
* Despite maximal medical measures, 15% of patients who initially survive an SAH experience stroke or death secondary
to vasospasm.
129
Large brain tumor elevates the cerebrospinal fluid pressure by decreasing ______ of the cerebrospinal fluid back into
the blood.
Large brain tumor elevates the cerebrospinal fluid pressure by decreasing reabsorption of the cerebrospinal fluid back into
the blood.
130
Hemorrhage or infection - number of red and/or white blood cells suddenly appear in the cerebrospinal fluid and can cause serious _____ of the small absorption channels through the ____ _________.
Hemorrhage or infection - number of red and/or white blood cells suddenly appear in the cerebrospinal fluid and can cause serious blockage of the small absorption channels through the arachnoidal villi.
131
Dementia Presentation (3):
1. _______ decline in cognitive abilities
2. Develops over ____ - _____
3. Predisposing factor for _____
Dementia Presentation (3):
Progressive decline in cognitive abilities
Develops over months - years
Predisposing factor for delirium
132
Post-op Cognitive Dysfunction (5):
1. Presents ____ – _____ after surgery
2. Memory _____
3. Difficulty _______
4. Impaired ______
5. Delayed _______ speed
Post-op Cognitive Dysfunction (5)
1. Presents **weeks – months** after surgery
2. Memory deficits
3. Difficulty concentrating
4. Impaired comprehension
5. Delayed psychomotor speed
133
Post-Op Delirium (5):
1. Immediately to _-_ days post-op
2. Fluctuating ______
3. Inattention
4. Memory _______
5. __________ abnormalities
Post-Op Delirium (5):
1. Immediately to 1-3 days post-op
2. Fluctuating consciousness
3. Inattention
4. Memory impairment
5. Perceptual abnormalities
134
Delirium Presentation (3):
1. Sudden change in _____ state
2. Develops over ____- ____
3. _______
Delirium Presentation (3):
1. Sudden change in mental state
2. Develops over days - weeks
3. Fluctuates
135
Delirium Predisposing factors (3):
1. Age above ____ years
2. ______ gender
3. _________
Delirium Predisposing factors (3):
1. Age above 70 years
2. Male gender
3. Dementia
136
Delirium Precipitating factors (4):
Delirium Prognosis:
_______ and _________
Delirium Precipitating factors (4):
1. Medications
2. Acute illness
3. Infections
4. Exacerbation of chronic medical illnesses
Delirium Prognosis:
Preventable and reversible
137
Delirium Etiology:
1. Accumulation of (3):
- ___ protein
- Beta-______
- alpha _______
2. Multiple _____ insults to the brain
Delirium Etiology:
1. Accumulation of (3):
- tau protein
- Beta-amyloid
- alpha synuclein
2. Multiple vascular insults to the brain
138
Delirium Pathophysiology:
1. Neuroinflammation
2. Reactive _______ species
3. ________ imbalance
4. Chronic ______
Delirium Pathophysiology:
1. Neuroinflammation
2. Reactive oxygen species
3. Neurotransmitter imbalance
4. Chronic stress
139
Delirium Prognosis:
Not reversible
EXCEPT in normal pressure
_____ & cases of
__________ resulting from B12 deficiency, thyroid disorders, syphilis, and depression
Delirium Prognosis:
Not reversible
EXCEPT in normal pressure
hydrocephalus & cases of
pseudodementia resulting from B12 deficiency, thyroid disorders, syphilis, and depression
140
Pseudodementia results from
1. ___ deficiency
2. ______ disorders
3. syphilis
4. depression
Pseudodementia results from
1. B12 deficiency
2. thyroid disorders
3. syphilis
4. depression
141
Dementia is now called
Major Neurocognitive Disorder (MND)
142
Dementia:
Can affect _______ individuals & does not always imply _______ disease as the etiology of cognitive decline.
Dementia:
Can affect younger individuals & does not always imply Alzheimer disease as the etiology of cognitive decline.
143
Dementia is characterized by a significant decline in at least ____ of the cognition domains:
* Executive function
* Complex attention
* Language
* Learning
* Memory
* Perceptual-motor
* Social cognition
Dementia is characterized by a significant decline in at least 1 of the cognition domains:
* Executive function
* Complex attention
* Language
* Learning
* Memory
* Perceptual-motor
* Social cognition
144
Dementia:
Decline represents a change from a patient's prior level of cognitive ability, is _____ and ______ over time, & not associated exclusively with
an episode of _____.
Also, must include decline in the patient's ability to _____ and perform _________ tasks.
Dementia:
Decline represents a change from a patient's prior level of cognitive ability, is **persistent and progressive** over time, & not associated exclusively with an episode of delirium.
Also, must include decline in the patient's ability to function and perform everyday tasks.
145
Dementia Etiology (13 etiological subtypes):
1. Alzheimer disease
2. Huntington disease
3. Vascular disease
4. Prion disease
5. Frontotemporal lobar degeneration
6. Substance and/or medication use
7. Lewy body disease 8. Traumatic brain injury
9. Parkinson disease 10. Another medical condition
11. HIV infection
12. Multiple etiologies
13. unspecified
Dementia Etiology (13 etiological subtypes):
1. Alzheimer disease
2. Huntington disease
3. Vascular disease
4. Prion disease
5. Frontotemporal lobar degeneration
6. Substance and/or medication use
7. Lewy body disease 8. Traumatic brain injury
9. Parkinson disease 10. Another medical condition
11. HIV infection
12. Multiple etiologies
13. unspecified
