ch 16: disorders of CNS, PNS, and NMJ Flashcards
1
Q
alterations of CNS function:
A
involve traumatic injury, vascular disorders, tumour growth, infections and inflammatory processes
2
Q
alterations of PNS function:
A
involve neural route, nerve plexus, nerves themselves, or neuromuscular junction
3
Q
traumatic brain injury
A
TBI is primary cause of death and disability in individuals under age of 40
- 30% of all TBIs are kids, are usually from sports and rec activities
4
Q
TBI (traumatic brain injury)
A
alteration in brain function or other evidence of brain disease caused by an external force
5
Q
primary TBI
A
- cause: indirect impact
- injury can be focal (affecting one area; 2/3) or diffuse (more than 1 area; 1/3; diffuse axonal injury, DAI)
6
Q
secondary TBI
A
- cause: indirect result of primary injury
- includes systemic responses and cascade of cellular and molecular cerebral events
7
Q
TBI diagnosis
A
glasgow coma scale (GCS)
8
Q
glasgow coma scale
A
3 categories:
1. eye (4)
2. verbal (5)
3. motor (6)
9
Q
GCS 2 scores
A
eye: eye opening to pain
verbal: incomprehensible sounds
motor: extension to pain
10
Q
GCS 3 scores
A
eye: eye opening to verbal command
verbal: inappropriate words
motor: flexion to pain
11
Q
classification scores
A
severe head injury: score of 8 or less
moderate head injury: score of 9-12
mild head injury: score of 13-15
12
Q
primary TBI
A
can be closed or open injury
- closed: more common, head sticking hard surface or moving object striking head, or blast waves, dura mater remains intact and brain tissue not exposed
- open: penetrating trauma or skull fracture, break in dura mater = brain tissue exposed
13
Q
types of primary TBI
A
- primary focal closed
- primary focal open
- primary diffuse injury
14
Q
types of primary focal closed TBIs
A
- coup/contrecoup
- contusion
- epidural (extradural) hematoma
- subdural hematoma
- intracerebral hematoma
15
Q
primary focal closed brain injury
A
specific, observable brain injuries that occur in a precise location
- mild: 80% of cases
- severe: contusions, epidural, subdural, and hematomas
16
Q
coup/contrecoup
A
coup = injury at site of impact
contrecoup = injury from brain bouncing back and hitting opposite side of skull
17
Q
contusions (brain bruising)
A
compression of skull at point of impact produces blood leaking from injured vessel
- contusion as a result of blood leaking from injured vessel
- smaller contact area = more severe the injury
- edema forms, increased ICP = hemorrhages, edema, infarction, necrosis = tissue becomes “pulpy”
- frontal lobed most common injury site
- greatest injury effects: peak 18-36 hours after injury
18
Q
contusions cont
A
- diagnosis: glasgow coma scale, CT scan, MRI
- TX: surgical removal of large contusions and areas of hemorrhage may be required
19
Q
TBI primary focal hematomas
A
- epidural
- subdural (acute, chronic)
- intracerebral
20
Q
epidural hematomas
A
- skull fracture
- hemiparesis
- pupil dilation
- loss of consciousness
21
Q
subdural hemotomas
A
acute: fast/hemianopia
chronic: alcohol/craniotomy, membrane forms around hematoma
22
Q
intracerebral hematomas
A
- frontal temporal
- penetrating sheering
- pupil dilation
- positive babinski
23
Q
epidural hematomas
A
bleeding between dura mater and skull
- artery bleeding and hematoma
- temporal fossa most common site of EH
24
Q
EH symptoms
A
- generally lose consciousness
- as hematoma grows = severe headache, confusion, seizure
- hemiparesis (weakness or inability to move one side of body)
- pupil dilation: injury prognosis good if treated before both pupils dilate
tx: medical emergency
25
dural
refers to dura mater
26
subdural hematomas
bleeding between dura mater and brain
- acute or chronic
27
acute SH
develop quickly, within hours
- hematomas grow, ICP rises, pressure is applied to bleeding veins (which assists in short term limitation)
symptoms: headache to confusion
- loss of consciousness, pupil dilation
- hemianopia = blindness over half of vision field
- anopia: aka blindness
28
chronic SH
develop over weeks to months
- common in alcohol abuse
- subdural mass bleeding = subdural space fills with blood
- vascular membrane forms around hematoma
symptoms:
- headaches and tenderness over hematomas
- worsening dementia, paratonia (rigidity)
TX: craniotomy to remove jelly-like blood
29
intracerebral hematomas
bleeding within the brain
- 2-3% of head injuries
- mainly in frontal and temporal lobes
- penetrating and shearing forces injure small blood vessels = growing mass/edema
symptoms:
- sudden rapid decrease in level of consciousness
- pupil dilation
- positive babinski reflex (big toe bends back and other toes fan out)
30
primary focal open TBI
compound skull fracture/missile injuries
31
compound skull fracture
opens a path between cranial contents and the environment
- whenever cuts of the scalp, tympanic membrane, sinuses, eye or mucous membranes occur a CSF sound be considered
32
causes of compound skull fractures
1. crush: cutting or crushing whatever missile touches
2. stretch: blood vessels and nerve damage without direct contact
33
compound skull fractures cont
- symptoms: become unconscious
basilar skull fractures:
- usually caused by substantial blunt force trauma
- involves one of the bones that compose the base of the skull
- general spinal fluid leaking from ear or nose, blackened eyes
34
primary diffuse injury
diffuse brain injury is widespread in brain
- effects from high levels of acceleration and deceleration (whiplash) or rotational forces
- forces cause shearing of axonal fibers and white matter tracts
- the degree of shearing determines the cognitive consequences and extensive cognitive impairments
extensive cognitive impairments (survivors of vehicle accidents)
diagnosis: electron microscope to detect axonal damage
35
secondary brain injury
indirect result of primary brain injury: including trauma and stroke syndromes
both systemic and cerebral processes involved:
- systemic: hypotension, hypoxia, etc.
- cerebral: inflammation, edema, increase ICP
36
secondary brain injury cont
primary effects cause disruption to BBB = neuronal death
management:
- prevention of hypoxia, maintenance of perfusion pressure, and removal of hematomas
37
categories of traumatic brain injury
1. mild
2. moderate
3. severe
38
mild TBI (mild concussion)
- characterized by immediate but transitory clinical manifestations
- loss of consciousness less than 30 minutes
- GCS (glasgow) score: 13-15
- symptoms: headache, nausea, vomiting
- diagnosis: blood test to determine need for CT scan
39
moderate TBI (moderate concussion)
- any loss of consciousness last more than 30 min up to 6 hrs
- GCS score 9-12
- permanent defects in arousal and attention
- symptoms: confusion and amnesia lasting more than 24 hours, brain imaging is abnormal
40
severe TBI (severe concussion)
characterized by loss of consciousness for more than 6 hours
- GCS score 3-8
- permanent damage to vegetative state to death
- signs: changes in pupillary reaction and cardiac and respiratory systems, decorticate or decerebrate posturing, brain imaging is abnormal, increased ICP occurs 4-6 days after injury
- symptoms: compromised coordinated movements, verbal and written communication
- goal of TX: maintain cerebral perfusion and promote neural protection
41
complications of TBI
severity/brain location determines the probable locations
3 post-traumatic syndromes:
1. post-concussion syndrome
2. post-traumatic seizures
3. chronic traumatic encephalopathy (CTE)
42
post-concussion syndrome
- can last weeks to months after concussion
- important to have first 24 hours of close observation
- symptoms requiring further evaluation: drowsiness, confusion, vomiting, unequal pupils, CSF drainage from ears or nose, double vision
43
post-traumatic seizures (epilepsy)
- 10-20% of TBIs
- highest risk with open brain injuries
- molecular changes = sprouting of new hyperexcitable neural activity = increased seizures
44
chronic traumatic encephalopathy (CTE)
- progressive dementing disease that develops with repeated brain injury
- associated with contact sports, and blast injuries with soldiers
- tau neurofibrillary tangles occur in brain
- consequences: violent behaviour, change in cognitive and motor function, depression, suicide
45
decorticate posturing
flexing arms towards core and center of body
46
decerebrate posturing
extension of arms
47
spinal cord and vertebral injury
at risk: male gender (20-39) and older adults (79+ - because of falls)
can be primary or secondary injury
48
primary spinal cord injury
- initial mechanical trauma = immediate tissue damage
- injury occurs if an injured spine does not receive adequate immobilization following trauma
- injury to C1- 4 = life threatening due to loss of CV and respiratory function
49
secondary spinal cord injury
- disease causing process (vascular, cellular, biochemical) occurring within minutes and continues for weeks
- hemorrhage appears in grey matter, result in death of entire grey matter at spinal level
- edema - impaired circulation = ischemia
- these symptoms occur at two cord segments above and below injury
- cord swelling = increased dysfunction = difficult to distinguish permanent and temporary damage
- death of oligodendrocytes = myelin degeneration
50
vertebral injuries
vertebral fractures, dislocation, bone fragments = shearing and compression
- vertebral fracture easily due to torn supporting ligaments
- vertebrae misalignment and dislocation occurs
- vertebral injuries occur at most moveable portions of column
51
hyperextension
disruption of intervertebral discs
- head moves up/back
- ligament compression and spinal cord compression
52
flexion
vertebral wedge fracture
- head moves down
- stretched ligaments
53
rotation
shearing force and rupture of ligament support
54
manifestations of spinal cord/vertebral injury
1. spinal shock
2. neurogenic shock
55
spinal shock
develops immediately after injury
- complete loss of function at or below level of injury
- hypothalamus cannot regulate body heat/person assumes temperature of aire (poikilothermic)
- generally lasts 7-20 days and returns with reflex emptying of bladder
56
neurogenic shock
occurs with injury above T6
- unopposed parasympathetic activity (due to absence of sympathetic activity)
- result: vasodilation, hypotension
57
primary headache syndrome
3 categories:
1. migraine
2. cluster
3. tension-type
58
migraine
- episodic, neurological headache lasting 4-72 hours
- genetic and environmental components
- classified as:
1. with aura
2. without aura
3. chronic
- occurrence in canada: 25% of women, 8% of men, 10% of children
59
aura
begins as spreading neural hyperactivity in occipital brain region (visual processing regions)
1/3 of persons have aura symptoms that last one to 1 hour
60
clinical phases of migraine
1. premonitory phase: symptoms occur hours to days before onset of aura (tired, irritable)
2. migraine aura
3. headache phase: begins on one side of head - spread to entire head
4. recovery phase: irritability, fatigue
61
cluster headache
headache involving trigeminal nerve
- pain may alternate sides each episode
- severe throbbing
- up to 8 attacks a day
- cluster days followed by long periods of remission
- primarily in men age 20-50
pathophysiology:
- pain related to neurogenic inflammation
- sympathetic underactivity and parasympathetic activation
TX: oxygen inhalation, sumatriptan
62
tension-type headaches
most common type of recurring headache
- age of onset: 10-20 years old
- gradual onset moves to sensation of tight band around head
- its is episodic over a period of days
- can develop into chronic if happening 15 days/month
- cause: hypersensitivity of pain fibers from trigeminal nerve
- TX: mild treated with ice, more severe treat with asprin
63
meningitis
infection of meninges and subarachnoid space
64
encephalitis
inflammation within brain
65
inflammation introduction
pathogens infect CNS
mechanism:
- direct neural or glial infection
- inflammation = edema
- interruption of CSF pathways
- secretion of toxins
66
bacterial meningitis
serious infections to which infants and children are susceptible
- streptococcus, s. pneumoniae and e coli are most common pathogens
- pathogens cross blood brain barrier, enter cerebrospinal fluid, multiply and release toxins
- ICP can occur due to blockage of CSF circulation
- progressive symptoms: spinal rigidity, seizures, positive babinski reflex
67
viral meningitis
may be direct infection or secondary to disease such as measles, mumps, or herpes
68
viral encephalitis
virus can directly invade brain and cause inflammation
- post-infection encephalitis may occur due to an autoimmune response
69
demyelinating disorders
1. multiple sclerosis (MS)
- CNS disorder
2. Guillian-Barr
- PNS disorder
70
what are demyelinating disorders
result of damage to myelin sheath
71
multiple sclerosis
chronic, immune-mediated inflammatory disease with CNS demyelination, scarring and loss of axons
- canada has one of the highest rates of MS
- onset: 20-40 yoa (more common in women)
- risk factors: epstein-barr virus (EBV), genetics
pathophysiology:
- diffuse progression in brain and spinal cord
- T and B cells cross BBB and attack myelin
- activation of microglia cells (CNS immune cells)
- result: death of neurons, brain atrophy with mainly white tissue atrophy
- gray matter degeneration occurs during later stages
manifestations:
- initial symptoms: paresthesia (burning or prickling sensations)
- exacerbation stages (relapses) followed by remission
- further exacerbations = progression of disease
TX:
- corticosteroids, immunosuppressants (both increased risk of infections)
- plasma exchange if patient doesn't respond to steroids
72
Guillain - Barre syndrome
pathophysiology:
- demyelination of peripheral nerves
- occurs secondary to respiratory or gastrointestinal infection
- recovery: weeks to years (30% have residual weakness)
symptoms:
- vary from tingling and weakness to leg paralysis, quadriplegia
73
NMJ disoder
myasthenia gravis
74
myasthenia gravis
most common NMJ disorder
- chronic autoimmune disease
- autoimmune: antibodies (IgG) against Ach receptors on postsynaptic membrane
- thymoma (tumour of thymus) associated with disorder
pathophysiology:
- AChR are not recognised as "self"
- result: Thymoma - formation of T-cell-dependant IgG autoantibodies which block binding site of AChR to ACh
- autoantibodies destroy receptor site
manifestation:
- muscles of head area earliest areas affected
- resulting dysphagia (difficulty swallowing) = risk of respiratory aspiration
- diaphragm and chest wall muscles weaken = impaired respiration
diagnosis:
- detection of anti-AChR antibodies
TX:
- immunosuppressants
- thymectomy for people with thymoma
75
brain tumours
can be primary or metastatic
76
oma
denotes tumor or cancer
77
primary tumours
arise from brain substance
- do not metastasize readily because there is no lymph channels in brain substance
- AKA primary intracerebral tumours and gliomas
- 50-60% of adult brain tumours
- ionizing radiation only known risk factor (ionizing radiation detaches electrons from other atoms as they pass through matter)
78
types of primary intracerebral tumours (gliomas)
1. astrocytoma
2. oligodendroglioma
3. meningioma
4. ependymoma
79
astrocytoma
most common
- grade III and IV = survival less than 5 years
80
oligodendroglioma
- slow growing (grade II)
- primarily in white matter
- seizure first symptom
81
meningioma
- begins in dura mater
- often located on wings of sphenoid bone
- seizures first symptom
82
ependymoma
- more common in children
- arise from ependymal cells with 70% of tumors begin in fourth ventricle
83
metastatic (secondary) tumours
arise in organ systems outside brain and spread to the brain
- local effects of tumours are compression causing decreased cerebral blood flow and increased ICP
- symptoms: seizures, visual disturbances
- 10 times more common than primary
- 20-40% of people who have cancer metastasis to brain
84
degenerative disorders of the spine
1. lower pack pain
2. degenerative disc disease (DDD)
3. herniated intervertebral disc
85
lower back pain
- affects area between lower rib cage and gluteal muscles (muscles of buttck area) with pain often radiating into the lower legs
- acute LBP associated with muscle or ligament strain
- chronic LBP includes degenerative disc disease, spondylolysis and spondylolisthesis
86
degenerative disc disease
process of normal aging, genetic
- spondylolysis
- spondylolisthesis
- spinal stenosis
87
spondylolysis
occurs in the pars interarticularis (between the superior and inferior articular processes)
- degeneration or fracture of this joint
88
spondylolisthesis
forward slippage of vertebrae
89
spinal stenosis
narrowing of spinal canal
- pressure on spinal nerves or cord
90
