Neuro of the CNS Flashcards
1
Q
What does brain injury change?
A
level of consciousness and alterations in cognitive, motor, and sensory function
2
Q
What is focal brain injury
A
focal neurologic deficits that may or may not alter consciousness.
3
Q
What is a global brain injury?
A
altered levels of consciousness, ranging from inattention to stupor or coma.
4
Q
Injury involving the _________ and _______ have a more predictable pattern
A
diencephalon, brainstem
5
Q
What are key clinical signs when it comes to brain lesions in the diencephalon, midbrain, pons, and medulla
A
- diencephalon: impaired consciousness, small reactive pupils, intact oculocephalic response, abnormal flexion posturing- cheyne- stoke respirations
- midbrain- coma, fixed midsize pupils impaired oculocephalic response, central nuerogenic hyperventialtion, extension posturing
- Pons- coma, fixed small pupils, disconjugate gaze, impaired oculovestibular response, loss of corneal reflex
- Medulla- coma, fixed pupils, flaccidity, loss of gaf and cough reflexes
6
Q
What is consciousness?
A
state of awareness of self and environment and of being able to orient to new stimuli
7
Q
What are the two divisions of consciousness?
A
(1) arousal and wakefulness: require function of both cerebral hemispheres and an intact reticular activating system (RAS)
(2) content and cognition: requires functioning cerebral cortex
8
Q
What is RAS?
A
is a network of neurons located in the brainstem that has fibers projecting to various parts of the brain
9
Q
What is the glascow coma scale?
A
- one way to measure altered status
-scale that is used in response to eye opening, motor response and verbal response and they are scored.
-best possible score is 15 and worst is 3
10
Q
Persistent Vegetative State
A
Loss of all cognitive functions and unawareness of self and surroundings. —Reflex and vegetative functions remain, including sleep–wake cycle
-sufficiently preserved hypothalamic and brain stem function; bowel and bladder incontinence
-variably preserved cranial nerve and spinal cord reflexes
11
Q
ICP is normally ≤
A
15 mmHg in adults
12
Q
Pathologic intracranial hypertension (ICH) is ≥
A
20 mmHg
13
Q
What are S/S of ICP?
A
HA, CN palsies, papilledema, Cushing triad
14
Q
What may ICP result in?
A
cerebral herniation, decreased perfusion, and secondary infarction of the affected areas
15
Q
What pathologies may cause an increase in the pressure of the closed system from ICP?
A
Cerebral Edema
Hydrocephalus
Intracranial mass lesions (eg, tumor, hemorrhage)
Obstruction of venous outflow (eg, venous sinus thrombosis, jugular vein compression
16
Q
What is cerebral edema?
A
Increased fluid leakage from blood vessels and injury to various cells of the CNS
17
Q
What is Vasogenic edema?
A
increase in extracellular fluid caused by BBB disruption and increased vascular permeability, allowing fluid to shift from the intravascular compartment -> intercellular spaces of the brain. Edema may be either localized or generalized
18
Q
What is Cytotoxic edema?
A
increase in intracellular fluid neuronal, glial, or endothelial cell membrane injury, i.e. generalized hypoxic/ischemic insult or with a metabolic derangement
19
Q
Hydrocephalus
A
-enlarged ventricular size
-Normal pressure
-excess CSF accumulation within ventricular system
from impaired flow or resorption of CSF
20
Q
What are the symptoms of Hydrocephalus?
A
Symptoms range from headache, visual changes, dementia, incontinance
21
Q
Papiledema
A
sign of increased ICP- symptom = visual changes
22
Q
Cerebral herniation
A
-Displacement of brain tissue past rigid dural folds or through openings in the skull because of increased intracranial pressure.
23
Q
What is cerebral herniation mostly caused by?
A
mass effects, either diffuse (generalized brain edema) or focal (tumors, abscesses, or hemorrhages)
24
Q
What are examples of trauma of the brain
A
- Parenchymal injury
Concussions, Contusion (edema and hemorrhage), lacerations - Diffuse Axonal Injury
- Vascular injury
Epidural, subdural, subarachnoid, Intraparenchymal
25
What is a Spontaneous (non-traumatic) Subarachnoid Hemorrhage?
rupture of a saccular (“berry”) aneurysm in a cerebral artery
26
What are the risk factors associated with Subarachnoid Hemorrhage?
-Genetics?
-Developmental anomalies?
-Smoking?
-Htn?
-Female, fifth decade
-Acute increase ICP
-Worst HA of life
-Sentinel bleed- "warning"
27
What is the most common types of vascular malformations?
Most common are:
1. arteriovenous malformations
Male predominance. Age 10-30
Middle cerebral artery most common territory
2. cavernous malformations
dilated, thin walled capillaries with a simple endothelial lining
28
What are the two types of cerebrovascular diseases?
aka stroke
1. Ischemic/hypoxic- embolism>>>thrombosis
2. Hemorrhagic
Tissue infarction is the ultimate consequence of both
One of leading cause of death in US
29
What is a stroke?
injury to the brain as a consequence of altered blood flow
1. Ischemic/hypoxic- embolism>>>thrombosis
2. Hemorrhagic
^^ tissue infarction is the ultimate consequence of both ^^
30
Penumbra
area of “at-risk” brain- region of transition between necrotic tissue and the normal brain
31
Lacunar infarct
Single deep penetrating arteries supplying the internal capsule, basal ganglia, or brain stem
32
Border zone (“watershed”) infarcts
the border zones between arterial territories
33
When blood flow to a portion of the brain is reduced, the survival of the tissue at risk depends on:
-collateral circulation- circle of willis
-Duration, magnitude and rapidity of the reduction of flow.
-These factors determine anatomic site, size of the lesion the clinical deficit.
34
What is hemorrhagic?
-Spontaneous (non-traumatic) rupture of a small intraparenchymal vessel -> primary hemorrhage within the brain, -> sudden onset of neurologic symptoms
middle to late adult life, with a peak incidence at about 60 y.o, Female
-Hypertension is most common risk factor
compression leads to secondary infarction of the affected brain tissue
35
What is Vascular Dementia defined by?
multiple, bilateral, gray matter (cortex, thalamus, basal ganglia) and white matter infarcts over course of months to years.
36
What are neurodegenerative diseases characterized by?
rupture of a small intraparenchymal vessel -> primary hemorrhage within the brain, -> sudden onset of neurologic symptoms
37
In which population does Hemorrhagic cerebrovascular disease most occur in
middle to late adult life, with a peak incidence at about 60 y.o
38
What is the most common risk factor of hemorrhagic cerebrovascular disease?
Hypertension
39
______ leads to secondary infarction of the affected brain tissue.
Compression
40
What is vascular dementia?
multiple, bilateral, gray matter and white matter infarcts over course of months to years. These appear with dementia like symptoms and in imaging it shows signs of silent/covert cerebrovascular brain injury, which indicates a vascular contribution to the dementia.
41
What is parkinson's disease marked by?
hypokinetic movement disorder that is caused by loss of dopaminergic neurons from the substantia nigra
42
What is clinical SYNDROME of parkinsonism?
-diminished facial expression (often termed masked facies)
-stooped posture
-slowing of voluntary movement
-festinating gait (progressively shortened, accelerated steps)
Rigidity
-“pill-rolling” tremor
43
What is the triad of parkinsonism?
tremor, rigidity, and bradykinesia
44
What is Parkinsons disease clinical impression confirmed by?
symptomatic response to L-Dopa replacement therapy
45
Mean onset age of Parkinson disease?
57 yo
46
In Parkinson's disease, the severity of the motor syndrome is proportional to________
dopamine deficiency
47
What is the pathogenisis of Parkinson's disease?
1. Lewy Body *diagnostic hallmark* -protein accumulation/aggregation w/in neurons - spherical, eosinophilic cytoplasmic inclusions
2. mitochondrial abnormalities
3. neuronal loss in the substantia nigra and elsewhere in the brain
48
What is the diagnostic hallmark of Parkinson's disease?
Lewy Body
49
Parkinsons disease involves the ________ and eventually progresses to involve the _________ leading to cognitive impairment.
lower brainstem
cerebral cortex
50
What are the characteristic features of Parkinsons disease?
fluctuating course, visual hallucinations, and prominent frontal signs
51
Huntiington's disease is an _________ dominant disease. No spoardiac form.
autosomal
52
What is the age of onset for Huntingon's disease?
40's-50s (depends on inherited pattern)
53
In Huntington's disease, the _______ symptoms often precede the ________
motor, cognitive impairment
54
Huntington's disease S/S
Chorea- Jerky, hyperkinetic, sometimes dystonic movements- whole body
later develop bradykinesia and rigidity.
55
What is the pathogenesis of huntington's disease?
-HTT (the gene for HD) encodes for a 348 kD protein known as Huntingtin.
-prototypic polyglutamine trinucleotide repeat expansion disease
- HTT gene contains 6 to 35 copies of repeat and when this number exceeds this, its associated with the disease.
-Parental transmission is associated with earlier onset in next generation
56
Where is atrophy frequently seen in HD?
caudate nucleus and putamen
57
What is Amyotrophic Lateral Sclerosis (ALS) ?
Progressive disorder marked by loss of upper motor neurons in the cerebral cortex and lower motor neurons in the spinal cord and brainstem
58
What does Amyotrophic Lateral Sclerosis (ALS) result in?
denervation of muscles, producing weakness that becomes profound as the disease progresses
59
Which population does ALS affect?
men slightly > women
Emerges in 50's or later
Sporadic ALS is more common than familial ALS
60
What occurs when the upper motor neurons are affected in ALS?
increased tone, hyperactive reflexes
61
What occurs when the lower motor neurons are affected in ALS?
muscle weakness, decreased tone, areflexia, fasciculations
62
What are the early symptoms of ALS
asymmetric weakness of the hands, manifested as dropping of objects and difficulty performing fine-motor tasks, and cramping and spasticity of the arms and legs
63
What are the later symptoms of ALS
muscle strength and bulk diminish, and fasciculations
64
ALS can eventually involve the respiratory muscles and lead to
pneumonia
65
In CNS demyelinating diseases, preferential damage to _______ occurs with preservation of _______. It is immune related and inherited.
myelin, axons
66
Multiple Sclerosis (MS) is an autoimmune _______ disorder
demyelinating
67
What is the most common demyelinating disorder?
Multiple Sclerosis (MS)
68
If the sx of a stroke lasts less than 24 hours it is called a
transient ischemic event
69
What is the function of upper motor neurons?
have inhibitory affect on muscles they tell muscles to stay relaxed, don’t contract
70
What is the function of lower motor neurons?
neurons are excitatory they make muscles contract
71
If you take out an upper motor neuron of a major extremity you are taking out _______ on that muscle so the muscle will be________
inhibitory tone, rigid
72
If you take out lower motor neuron then that muscle group will be_______
flaccid
73
Distinctive clinical _______ may be caused by any cerebrovascular or cardiovascular disease that leads to vascular brain injury or dysfxn
syndrome
74
Which disease is the second most common form of dementia after Alzheimers?
Vascular Dementia
75
Neurodegenerative diseases are disorders characterized by the ____________, which often have ______functions.
progressive loss of particular groups of neurons, shared
76
What is the common pathologic process in neurodegenerative disease?
accumulation of protein aggregates and are resistant to degradation and show aberrant localization within neuron
77
What are the 3 factors that vary among the spectrum of neurodegenerative disease?
1. etiology of aggregation
2. Anatomic location
3. specific cellular abnormalities (e.g., tangles, plaques, Lewy bodies)
78
Which disease is the most common cause of dementia in older adults?
Alzheimer Disease (AD)
79
In Alzheimer Disease (AD), patients have an accumulation of _________ in specific brain regions which is a result of excessive production and defective removal.
2 proteins:
1.Aβ
2. tau
80
In Alzheimer Disease (AD), amyloid plaques (aggregated Aβ peptides) and neurofibrillary tangles (tau) trigger an ________ response and burden load correlates with _________
inflammatory, cognitive impairment
81
One of the genetic changes associated with AD occurs on __________ which is the same chromosome affected in Down syndrome.
chromosome 21
82
In Alzheimer Disease (AD), the brain shows variable ____________ marked by _______narrowing and _______widening that is most pronounced in the frontal, temporal, and parietal lobes
cortical atrophy
gyral
sulcal
83
In AD, which structures in the medial temporal lobe are involved early in the disease course?
hippocampus, amygdala
84
Parkinson Disease (PD) is the most common cause of ________
parkinsonism
85
Huntington Disease (HD) is a progressive and is uniformly ________ > average course of about _____ years
fatal, 15
86
In ALS, there is toxic protein accumulation involved in degeneration of the ______ and __________
UMN
LMN
87
Which population does MS mostly affect?
women
88
In MS, there are neurologic deficits that are separated in time which means that the patient has ______ and ______ episodes of neurologic defects of variable duration (weeks to months). The frequency of relapses decreases over time but there is _________ deterioration in most affected individuals.
relapsing, remitting
steady
89
What is the frequent manifestation of MS?
1. Unilateral visual impairment (optic neuritis- involvement of the optic nerve
2. involvement of brainstem produces cranial nerve signs (ataxia, nystagmus)
3. leg paresis/paresthesias
90
In MS, what do spinal cord lesions give rise to?
motor and sensory impairment of trunk and limbs, spasticity, and loss of bladder control
90
In MS, what do spinal cord lesions give rise to?
motor and sensory impairment of trunk and limbs, spasticity, and loss of bladder control
91
What would you most likely see in the CSF in a patient with MS?
mildly elevated protein level
92
Describe what an active plaque causes in MS
ongoing myelin breakdown associated with abundant foamy macrophages. Lymphocytes are also present, mostly as perivascular cuffs, especially at the outer edge of the lesion
93
Describe what an inactive plaque causes in MS?
reactive gliosos: inflammatory cells gone; little to no myelin is found; reduction in the number of oligodendrocyte nuclei; instead, reactive gliosis is prominent.
94
In childhood, CNS tumors occur in _______ while in adults, arise in the ___________
posterior fossa,
cerebral hemispheres
95
Which is the most common group of primary brain tumors?
gliomas: astrocytomas, oligodendrogliomas, and ependymomas
96
Infiltrating _________ and _________ accounts for most primary brain tumors in adults. They are usually found in _________ and often occur in _______ through ______ decades
astrocytoma and glioblastoma
cerebral hemispheres
4th- 6th
97
What are meningiomas?
predominantly benign tumors of adults. Arise from the meningothelial cells of the arachnoid and are usually attached to the dura
98
What are the most common primary sites of metastatic lesions?
lung, breast, skin (melanoma), kidney, and gastrointestinal tract, accounting for about 80% of all metastases combined
99
Pituitary Adenoma
visual impairment/diplopia/headache or hormonal abnormalities
100
Infection may damage the nervous system directly through
1. Directly through injury of neurons or glia by the infectious agent
2. Indirectly through microbial toxins
3. destructive effects of the inflammatory response
4. as a result of immune-mediated mechanisms.
101
What are the 4 principal routes of CNS infections?
1. Hematogenous spread
2. Direct implantation
3. Local extension
4. Peripheral nervous system
102
What is the pathogenisis of emeningitis?
bacteria replicate and undergo lysis in the CSF, releasing endotoxins or cell wall fragments. These initiate release of inflammatory mediators, which permits pathogens, neutrophils, and albumin to move across the capillary wall into the CSF
103
How meningeal irritation and neurologic impairment present?
fever, headache, photophobia, irritability, clouding of consciousness, and neck stiffness.
104
What is a spinal tap?
cloudy or frankly purulent CSF
increased CSF pressure
increased protein concentration,
markedly reduced glucose content.
105
What is a seizure?
a single event of abnormal discharge that results in an abrupt, altered state of function
106
______ is a chronic disorder of recurrent seizures
Epilepsy
107
What do the manifestations of seizure disorders typically include?
sensory, motor, autonomic, or psychic phenomenon
108
What can seizures occur as a result of?
an underlying systemic illness, metabolic derangement, head injury, vascular event, tumor, etc.
109
What are the 2 classifications of Seizures?
1. Focal seizures
specific area of the cerebral hemisphere
no impairment of consciousness (aware) or with impaired consciousness (impaired awareness).
2. Generalized seizures
involve both cerebral hemispheres.
Loss of consciousness
varying bilateral degrees of symmetric motor responses without localization to one hemisphere.
divided into motor and nonmotor.
110
Focal seizures can be one of two things:
1. focal onset without impairment of consciousness or awareness
2. focal onset with impairment of consciousness or awareness
111
What are the motor class of seizures?
1. Tonic–Clonic (Grand-Mal)
Incontinence, tongue biting, airway compromise, post-ictal
2. Myoclonic
brief involuntary muscle contractions
3. Clonic
sudden hypotonia. This is followed by limb jerking
4. Tonic
Sudden increased tone, in the extensor muscles. associated with falling.
5. Atonic
Drop attacks
112
What are non motor seizures?
-Absence Seizures
-Generalized & nonconvulsive
mainly disturbances in consciousness
-Mostly pediatric
-may cease or evolve
-blank stare, motionlessness, and unresponsiveness
lip smacking, mild clonic motion (usually in the eyelids)
-changed postural tone, and autonomic phenomena
113
What is Status Epilepticus?
-Seizures that do not stop spontaneously or occur back to back without recovery
-Life threatening emergency -> respiratory failure and death
-If status epilepticus is caused by neurologic or systemic disease, must treat underlying cause to stop seizure activity
