Neuro Pathophysiology PPT

Question 1

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

Answer 1

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

Question 2

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 ______ _________

Answer 2

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

Question 3

Pathophysiology of Major Neurocognitive Disorder:

Accumulation of native _____ in the brain
(except vascular)

Answer 3

Pathophysiology of Major Neurocognitive Disorder:

Accumulation of native proteins in the brain
(except vascular)

Question 4

Vascular dementia ~____% of all dementia cases
* Incidence increases with ___
* Doubles every _____ years
* Risk factors (4):

Answer 4

Vascular dementia ~15% of all dementia cases
* Incidence increases with age
* Doubles every 5.3 years
* Risk factors - hypercholesteremia, diabetes
mellitus, hypertension, and smoking

Question 5

Lewy body dementia ___% of dementia cases

Answer 5

Lewy body dementia: ~5% of dementia cases

Question 6

Parkinson disease dementia ___% of cases of
dementia

Answer 6

• Parkinson disease dementia 10% of cases of
  dementia

Question 7

Frontotemporal dementia ~___% of dementia
cases in patients older than ____ years of age

Answer 7

Frontotemporal dementia ~25% of dementia
cases in patients older than 65 years of age

Question 8

Dementia-type diseases:
Cause _______ damage to various areas of your brain, causing _______ in
several areas of the brain to die

Answer 8

Dementia-type diseases:
Cause progressive damage to various areas of your brain, causing neurons in
several areas of the brain to die

Question 9

Dementia-type diseases: (5)

Answer 9

• Alzheimer’s disease
• Frontotemporal dementia
• Chronic traumatic encephalopathy (CTE)
• Lewy body dementia
• Limbic predominant age-related TDP-43 encephalopathy
  (LATE)

Question 10

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.

Answer 10

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.

Question 11

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 ______.

Answer 11

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.

Question 12

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

Answer 12

• 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

Question 13

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 _________ ______

Answer 13

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

Question 14

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

Answer 14

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

Question 15

Risk factors for Alzheimer’s (6):

Answer 15

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

Question 16

_______, _________, & ________ increase risk
for developing dementia & progression of Alzheimer’s

Answer 16

Hypertension, diabetes, & hyperlipidemia increase risk for developing dementia & progression of Alzheimer’s

Question 17

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.

Answer 17

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.

Question 18

Promising pharmacological treatments for Alzheimer’s are poised at
advanced stages of clinical trials and include (3)

Answer 18

anti-amyloid β
anti-tau
anti-inflammatory strategies.

Question 19

Clinical Phases of Alzheimer’s:

1. Pre-clinical or the pre-symptomatic stage:

• mild _______ loss
• early pathological changes in ______ and ________
• no functional impairment in _____
• absence of clinical signs and symptoms

Answer 19

Clinical Phases of Alzheimer’s:

1. 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

Question 20

Clinical Phases of Alzheimer’s:

2. 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 ________

Answer 20

Clinical Phases of Alzheimer’s:

2. 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

Question 21

Clinical Phases of Alzheimer’s:

3. Moderate stage
   * disease spreads to _______ ______ areas
   * increased memory loss
   * trouble _________
   * loss of ______ control
   * difficulty in ______, ______, and ______

Answer 21

Clinical Phases of Alzheimer’s:

3. 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

Question 22

Clinical Phases of Alzheimer’s:

4. 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 ____

Answer 22

Clinical Phases of Alzheimer’s:

4. 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

Question 23

Frontotemporal Dementia
Neurodegenerative disorder is a spectrum of clinical syndromes
characterized by ______ degeneration involving the ______ and
_____ ________ lobes of the brain

Answer 23

Frontotemporal Dementia
Neurodegenerative disorder is a spectrum of clinical syndromes
characterized by neuronal degeneration involving the frontal and
anterior temporal lobes of the brain

Question 24

Frontotemporal Dementia
Neurodegenerative disorde :

Clinical manifestations (5):

Etiology (2):

Answer 24

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

Question 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):

Answer 25

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

Question 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

Question 27

Frontotemporal Dementia
Neurodegenerative disorder:

Treatment (2 categories):

Answer 27

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)

Question 28

Frontotemporal Dementia
Neurodegenerative disorder

Pharmacologic Treatment:

Answer 28

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)

Question 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):

Answer 29

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

Question 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

Answer 30

Multiple Sclerosis (MS)

Question 31

Common demyelinating diseases that
affect your central nervous system
(brain and spinal cord) include (6):

Answer 31

• 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).

Question 32

Multiple Sclerosis (MS) attacks what anatomical structures (3):

Answer 32

• myelin
• oligodendrocytes (myelin producing cells)
• underlying nerve fibers

Question 33

Multiple
Sclerosis (MS) Symptoms (11):

Answer 33

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

Question 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 ______ & _______

Answer 34

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

Question 35

Multiple
Sclerosis (MS) Diagnosis (3):

Answer 35

a) MRI
b) Elevated IgG in the cerebrospinal fluid
c) Decreased conduction velocity on evoke potential studies

Question 36

Treatment of Multiple
Sclerosis (MS):

__________ agents directed toward reducing
formation of new lesions & decreasing incidence of relapse

Answer 36

Treatment of Multiple
Sclerosis (MS):

Immunomodulatory agents directed toward reducing
formation of new lesions & decreasing incidence of relapse

Question 37

Multiple Sclerosis (MS) Risk Factors (6):

Answer 37

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

Question 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

Answer 38

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

Question 39

Multiple Sclerosis Anesthesia Considerations:

T/F

There is NO evidence to support the use of one inhaled or injected anesthetic drug over another

Answer 39

Multiple Sclerosis Anesthesia Considerations:

TRUE

There is NO evidence to support the use of one inhaled or injected anesthetic drug over another

Question 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

Answer 40

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

Question 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

Answer 41

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

Question 42

Multiple Sclerosis Anesthesia Considerations:

• Corticosteroid supplementation – consideration in patients on long-term corticosteroids

Answer 42

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

Question 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

Answer 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 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

Question 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

Answer 44

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

Question 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

Answer 45

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

Question 46

Common demyelinating diseases that
affect your peripheral nervous system
include (3):

Answer 46

• Guillain-Barré
  syndrome (GBS)
• Charcot-Marie-Tooth
  disease (CMT)
• Chronic inflammatory
  demyelinating
  polyneuropathy (CIDP)

Question 47

Guillain-Barré
syndrome (GBS):

Occurring at a rate of 1-2 cases/100,000 persons per
year worldwide
* Increases with ____
* More prevalent in ___

Answer 47

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

Question 48

Most common variant of GBS

Answer 48

Acute Inflammatory demyelinating polyneuropathy (AIDP)

Question 49

GBS Symptoms:

affect ______ nerves resulting in clinical triad:

Answer 49

GBS Symptoms:

affect cranial nerves resulting in clinical triad:

*ophthalmoplegia
*ataxia
*areflexia

Question 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

Answer 50

?????

Question 51

Stroke Risk factors (8):

Answer 51

• Hypertension
• Diabetes
• Smoking
• Atherosclerosis
  Stroke-related disorders of the cerebrovascular system
• atherosclerotic disease of the carotid artery
• cerebral aneurysm
• arteriovenous malformation
• moyamoya disease.

Question 52

Blood supply to the brain is via two pairs of vessels:

Answer 52

• internal carotid arteries
• vertebral arteries

Question 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.

Answer 53

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.

Question 54

Carotid arteries vessels comprise the ______ circulation (5):

Answer 54

Carotid arteries vessels comprise the anterior circulation (5):

• Frontal
• Parietal
• lateral temporal lobes
• basal ganglia
• most of the internal capsule

Question 55

Vertebral arteries each give rise to a ______-______ cerebellar artery before converging at the level of the _____ to form the
_______ artery

Areas (5):

Answer 55

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

Question 56

Ischemic Stroke

Prognosis depends on the _____ _______ from the onset of symptoms to thrombolytic intervention if thrombosis is the cause
of the symptoms.

Answer 56

Ischemic Stroke

Prognosis depends on the time elapsed from the onset of symptoms to thrombolytic intervention if thrombosis is the cause
of the symptoms.

Question 57

An ischemic stroke is the result of an _______ of a vessel that supplies a region of brain resulting in cellular ______ and subsequent
cellular ________.

Answer 57

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.

Question 58

Parkinson’s Disease:

Nonmotor Features (4):

Answer 58

Parkinson’s Disease:

Nonmotor Features:

1. sleep disturbances
2. depression and anxiety
3. autonomic dysfunction
4. cognitive impairment in advanced stages

Question 59

Parkinson’s Disease – paralysis agitans:

Widespread degeneration of the portion of the _______ ______ that
sends _________ secreting nerve fibers to the _____ ______ and ________.

Answer 59

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.

Question 60

Parkinson’s Disease:

_______ is presumed to inhibit the rate of firing of the neurons that control the _________ motor system.

Answer 60

Parkinson’s Disease:

Dopamine is presumed to inhibit the rate of firing of the neurons that control the extrapyramidal motor system.

Question 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 __________

Answer 61

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

Question 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 ______

Answer 62

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

Question 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

Answer 63

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

Question 64

Parkinson’s Disease:

Involuntary Tremor:

feedback circuits ______ because of high
feedback gains after loss of their inhibition (occurs during all ______ hours)

Answer 64

Parkinson’s Disease:

Involuntary Tremor:

feedback circuits oscillate because of high feedback gains after loss of their inhibition (occurs during all waking hours)

Question 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

Answer 65

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

Question 66

Parkinson’s Treatment:

Goal of therapy: increase concentrations of ______ in the basal ganglia or
decrease the neuronal effects of ____________

Answer 66

Parkinson’s Treatment:

Goal of therapy: increase concentrations of dopamine in the basal ganglia or
decrease the neuronal effects of acetylcholine

Question 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

Question 68

Huntington’s Disease:

___________ ________ hereditary disease – trinucleotide repeats in the gene for Huntington’s

Answer 68

Huntington’s Disease:

Autosomal dominant hereditary disease – trinucleotide repeats in the gene for Huntington’s

Question 69

________ is characterized by sudden neurologic deficits
resulting from ischemia (____% of cases) or hemorrhage
(____% of cases).

Answer 69

Stroke is characterized by sudden neurologic deficits
resulting from ischemia (88% of cases) or hemorrhage
(12% of cases).

Question 70

The anterior and posterior circulations communicate via the _______
communicating artery, and the left and right ______ cerebral arteries
communicate via the _______ communicating artery.

Answer 70

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.

Question 71

T/F

Occlusion of specific arteries distal to the Circle of Willis results in predictable clinical neurologic deficits.

Answer 71

TRUE

Question 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

Answer 72

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

Question 73

Risk of acute ischemic stroke (6):

Answer 73

• Systemic hypertension - most significant risk factor
• Cigarette smoking
• Hyperlipidemia
• Diabetes mellitus
• Excessive alcohol consumption
• Increased serum homocysteine
  concentrations

Question 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

Answer 74

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

Question 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)

Answer 75

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)

Question 76

Intraparenchymal Hemorrhage:

Answer 76

bleeding that occurs within the brain’s functional tissue, or parenchyma

Question 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

Answer 77

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

Question 78

Subdural Hemorrhage:

Blood accumulation between ____ _____ & ______ layer - Rupture of bridging veins that run in the _____ space

Answer 78

Subdural Hemorrhage:

Blood accumulation between dura mater & arachnoid layer - Rupture of bridging veins that run in the subdural space

Question 79

Cerebral aneurysm are abnormal, localized ______ of the intracranial arteries

Answer 79

Cerebral aneurysm are abnormal, localized dilations of the intracranial arteries
Classifications
* Berry
* Mycotic
* Traumatic
* Fusiform
* Neoplastic
* Atherosclerotic

Question 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

Answer 80

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

Question 81

Subarachnoid hemorrhage

Signs & Symptoms (7):

Answer 81

Subarachnoid hemorrhage

Signs & Symptoms (7):

• Intense headache
• Transient loss of consciousness
• Nausea & vomiting
• Photophobia
• Fever
• Meningism
• Focal neurological deficits

Question 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.

Answer 82

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.

Question 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)

Question 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

Question 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

Question 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.

Question 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.

Question 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.

Question 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

Question 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

Question 91

Causes of Increased ICP (5):

Answer 91

*Aqueductal stenosis
*Benign intracranial hypertension
*Normal pressure hydrocephalus
*Intracranial Hemorrhage
*IIntracranial tumors

Question 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

Question 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

Question 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.

Question 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

Question 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
3. 0.25 – 1 g/kg
4. Transient vasodilation – increase CBF – increase ICP
5. Begin 30 minutes, maximum effect 1 to 2 hours, & last up to 6 hours
6. 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

Question 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)

Question 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

Question 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

Question 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

Question 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

Question 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)

Question 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

Question 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

Question 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.

Question 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

Question 107

Astrocytoma

Astrocytic tumors typically show diffusely infiltrating fibrillary glial cells with a microcytic background
and regional heterogeneity.

Question 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.

Question 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

Question 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

Question 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

Question 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

Question 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

Question 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

Question 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

Question 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

Question 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

Question 118

Stroke Etiologies (5):

Answer 118

• 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

Question 119

Stroke Diagnosis (3):

Answer 119

• 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

Question 120

Stroke Intervention Goal:

Answer 120

Goal: Restoring blood flow to ischemic penumbra & avoiding secondary cerebral damage

Question 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

Answer 121

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

Question 122

Extradural Hemorrhage Symptoms:

*Progressive alteration in _____
* Increased ____
* Decreased ____

Treatment:
* Excellent prognosis with early ________ evacuation

Answer 122

Extradural Hemorrhage Symptoms:

*Progressive alteration in consciousness
* Increased ICP
* Decreased CPP

Treatment
* Excellent prognosis with early hematoma
evacuation

Question 123

Subdural Hemorrhage:

Etiology (2):

Signs & symptoms (5):

Answer 123

Subdural Hemorrhage:

Etiology:
* Trauma
* Anticoagulant therapy

Signs & symptoms:
* Drowsiness
* Obtundation
* Hemiparesis
* Hemianopsia
* Language disturbances

Question 124

Subdural Hemorrhage Treatment (4):

Answer 124

Treatment:
* Conservative medical stabilized condition
* Evacuation of hematoma
* Drained via Burr holes
* Craniotomy

Question 125

Arteriovenous
Malformation:

Congenital intracerebral networks – ______ flow directly into _____

*Lack ability to ________

Answer 125

Arteriovenous
Malformation:

Congenital intracerebral networks – arteries flow directly into veins

*Lack ability to autoregulate

Question 126

Arteriovenous
Malformation:

Signs & Symptoms (5):

Diagnosis (1):

Answer 126

Arteriovenous
Malformation
Signs & Symptoms:
* Headache
* New focal neurologic deficits
* Acute hemorrhage
* Seizures
* Hydrocephalus or macrocephaly

Diagnosis - MRI

Question 127

Severity of a subarachnoid hemorrhage (SAH) can be graded clinically with either the _____ & _____ or World Federation Surgeons Scale (Nagelhout; page 734)

Answer 127

Severity of a subarachnoid hemorrhage (SAH) can be graded clinically with either the Hunt & Hess or World Federation Surgeons Scale (Nagelhout; page 734)

Question 128

Despite maximal medical measures, ____% of patients who initially survive an SAH experience stroke or death secondary
to __________.

Answer 128

• Despite maximal medical measures, 15% of patients who initially survive an SAH experience stroke or death secondary
  to vasospasm.

Question 129

Large brain tumor elevates the cerebrospinal fluid pressure by decreasing ______ of the cerebrospinal fluid back into
the blood.

Answer 129

Large brain tumor elevates the cerebrospinal fluid pressure by decreasing reabsorption of the cerebrospinal fluid back into
the blood.

Question 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 ____ _________.

Answer 130

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.

Question 131

Dementia Presentation (3):

1. _______ decline in cognitive abilities
2. Develops over ____ - _____
3. Predisposing factor for _____

Answer 131

Dementia Presentation (3):

Progressive decline in cognitive abilities

Develops over months - years

Predisposing factor for delirium

Question 132

Post-op Cognitive Dysfunction (5):

1. Presents ____ – _____ after surgery
2. Memory _____
3. Difficulty _______
4. Impaired ______
5. Delayed _______ speed

Answer 132

Post-op Cognitive Dysfunction (5)

1. Presents weeks – months after surgery
2. Memory deficits
3. Difficulty concentrating
4. Impaired comprehension
5. Delayed psychomotor speed

Question 133

Post-Op Delirium (5):

1. Immediately to - days post-op
2. Fluctuating ______
3. Inattention
4. Memory _______
5. __________ abnormalities

Answer 133

Post-Op Delirium (5):

1. Immediately to 1-3 days post-op
2. Fluctuating consciousness
3. Inattention
4. Memory impairment
5. Perceptual abnormalities

Question 134

Delirium Presentation (3):

1. Sudden change in _____ state
2. Develops over ____- ____
3. _______

Answer 134

Delirium Presentation (3):

1. Sudden change in mental state
2. Develops over days - weeks
3. Fluctuates

Question 135

Delirium Predisposing factors (3):

1. Age above ____ years
2. ______ gender
3. _________

Answer 135

Delirium Predisposing factors (3):

1. Age above 70 years
2. Male gender
3. Dementia

Question 136

Delirium Precipitating factors (4):

Delirium Prognosis:
_______ and _________

Answer 136

Delirium Precipitating factors (4):

1. Medications
2. Acute illness
3. Infections
4. Exacerbation of chronic medical illnesses

Delirium Prognosis:
Preventable and reversible

Question 137

Delirium Etiology:

1. Accumulation of (3):
   - ___ protein
   - Beta-______
   - alpha _______
2. Multiple _____ insults to the brain

Answer 137

Delirium Etiology:

1. Accumulation of (3):
   - tau protein
   - Beta-amyloid
   - alpha synuclein
2. Multiple vascular insults to the brain

Question 138

Delirium Pathophysiology:

1. Neuroinflammation
2. Reactive _______ species
3. ________ imbalance
4. Chronic ______

Answer 138

Delirium Pathophysiology:

1. Neuroinflammation
2. Reactive oxygen species
3. Neurotransmitter imbalance
4. Chronic stress

Question 139

Delirium Prognosis:

Not reversible
EXCEPT in normal pressure
_____ & cases of
__________ resulting from B12 deficiency, thyroid disorders, syphilis, and depression

Answer 139

Delirium Prognosis:

Not reversible
EXCEPT in normal pressure
hydrocephalus & cases of
pseudodementia resulting from B12 deficiency, thyroid disorders, syphilis, and depression

Question 140

Pseudodementia results from

1. ___ deficiency
2. ______ disorders
3. syphilis
4. depression

Answer 140

Pseudodementia results from

1. B12 deficiency
2. thyroid disorders
3. syphilis
4. depression

Question 141

Dementia is now called

Answer 141

Major Neurocognitive Disorder (MND)

Question 142

Dementia:

Can affect _______ individuals & does not always imply _______ disease as the etiology of cognitive decline.

Answer 142

Dementia:

Can affect younger individuals & does not always imply Alzheimer disease as the etiology of cognitive decline.

Question 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

Answer 143

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

Question 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.

Answer 144

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.

Question 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
8. Parkinson disease 10. Another medical condition
9. HIV infection
10. Multiple etiologies
11. unspecified

Answer 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
8. Parkinson disease 10. Another medical condition
9. HIV infection
10. Multiple etiologies
11. unspecified