CNS Disorders Flashcards
1
Q
Types of CNS Disorder
A
- These are disorders within the brain and spinal cord
- Traumatic Brain Injury (TBI)
- Strokes
- Infections – Meningitis, Encephalitis
- Seizures
- Tumors
- Spinal Cord Injuries
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Q
Layers of Meninges of the Brain
A
Dura Mater (outer layer)
Arachnoid
Pai Mater (inner layer)
3
Q
Respiratory Center in the Brain Stem
A
- Inspiratory Area (Medulla)
- Stimulates the muscles of inspiration and eventually the pneumotaxiccenter
- Expiratory Area (Medulla)
- Inhibits the inspiratory center (mostly during high RR, and Vt.)
- Apneustic Area (Pons)
- Stimulates the inspiratory center
- Pneumotaxic Area (Pons)
- Inhibits apneusticand inspiratory center and allows exhalation
4
Q
Central Neurogenic Hyperventilation
A
May be the result of compression of the mid-brain from edema or trauma
5
Q
Central Neurogenic Apnea
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Total loss of all respiratory drive
Destruction of the entire respiratory drive center
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Q
Biot’s Breathing
A
- Characterized by short episodes of rapid uniformly deep inspiration followed by periods of 10 to 30 seconds of apnea
- Caused by damage to, or pressure on, the medulla
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Q
Apneustic Breathing
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- Prolonged insp. gasping
- Pons damage
8
Q
Central Reflex Hyperpnea
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Continuous deep breathing
Pons damage
9
Q
Central Reflex Hypopnea
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•Head trauma, brain hypoxia, narcotic suppression
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Q
Cheyne-Stokes Breathing
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- Cycles of gradual increase in rate and volume followed by gradual decrease, then a period of apnea before it repeats
- Associated with decreased cardiac output (heart failure), central sleep apnea, and damage to respiratory centers
11
Q
Kussmaul’s Breathing
A
Rapid and deep breaths associated with metabolic (often diabetic keto-acidosis),not neurogenic.
12
Q
Cerebral Blood Flow and CO2
A
Mediated through formation of H+
CO2 dilates brain vessels = CBF
Ventilation strategies include low-normal PaCO2 to ¯CBF and ¯ICP
Temporarily we may hyperventilate more than this but the disadvantage is decreased oxygen delivery to the brain
13
Q
Cerebral Blood Flow and ICP
A
Normal ICP is 10-15 mmHg
Small fluctuations normal; variability > 10 mmHg a bad sign
At 15-20 mmHg capillary bed is compressed and microcirculation is compromised; > 20 mmHg is intracranial hypertension
At 30-35 mmHg venous drainage is impeded and edema develops in uninjured tissue
CPP = MAP – ICP
ICP increase of 1 mmHg= Decrease CBF by 0.5-0.7 mL
PaCO2 decrease of 1 mmHg=3% decreased in CBF
PaCO2¯of 1 mm Hg = 3% ¯in CBF
14
Q
Traumatic Brain Injury
A
–Damage to the brain caused by external mechanical force
–Can be classed by severity, location (e.g. subdural hematoma), mechanism (closed vs. open)
TBI is a major cause of death and disability world wide!
Disabilities extend from the physical to include impact on cognitive, social, emotional and behaviouralfunctions.
15
Q
Traumatic Brain Injury
Major Causes
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- MVC/motorbikes
- Sports related
- Falls
- Violence/abuse
16
Q
TBI- Mild Injury
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- Glasgow Coma Scale 13-15, loss of consciousness up to 15 minutes
- Usually recover
17
Q
TBI- Moderate Injury
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- GCS 9-12, LOC up to 6 hours, may deteriorate because of rising ICP
- CT scan useful but may not need hemodynamic or respiratory support
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Q
TBI- Severe Injury
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- GCS 3-8, LOC over 6 hours, CT scan to identify extent of damage
- Respiratory and circulatory support usually needed
19
Q
Combative Patient
A
Combative patients may need to be heavily sedated to acquire a CT scan, necessitating intubation.
20
Q
TBI- Mild Injury
Signs and Symptons
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Headache, nausea and vomitting, lack of motor coordination, dizziness, clumsiness, visual disturbances, changes in sleep patterns
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Q
TBI- More Severe Injury
Signs and Symptons
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- Loss of consciousness
- Dilation of one or both pupils; blown pupils
- Respiratory depression
- Cushing’s triad: slow heart rate, high blood pressure and respiratory depression a sign of high ICP
- Paralysis/weakness
22
Q
Cushing’s Traid
A
Cushing’s triad: slow heart rate, high blood pressure and respiratory depression a sign of high ICP
23
Q
TBI and Posturing
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- Damage to the cerebrum may cause decorticate posturing.
- Arms, wrists and fingers will be flexed (bent in on themselves) and adducted (turned inward)
- Legs will be rigid and straight (extended), feet rotated inward
- Damage to the brain stemmay cause decerebrate posturing
- Arms are extended and rotated inward
- Legs and feet are rigid and hyper-extended
24
Q
Epidural Hemotoma
A
–Accumulation of blood between the skull and the outer duralayer. Usually from impact type trauma.
–May be rupture of the meningeal artery. Victim may fair well at first and then deteriorate rapidly as fluid accumulates.
–Treatment is immediate cerebral drainage (burr hole).
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Sub Dural Hematoma
* Accumulation of blood between theduraand arachnoid layers
* Usually acceleration/ deceleration injury that caused rupture of cerebral veins
* Typed by onset of symptoms:
* Acute: within 48 hours of injury
* Sub-acute: 3 to 20 days
* Chronic: 20 or more days post injury
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Intracerebral Hematoma
–Blood in the parenchyma of the brain, could be from any of the previous types of traumas
–Ventricles fill with blood and enlarge, displacing other tissues
–Immediately life threatening
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TBI
Penetrating Injuries
–E.g. knives, bullets, projectiles
–Obviously life-threatening
–Vascular tearing as projectile enters the skull
–Small caliber bullets tend to ricochet around inside the skull and leave no exit wound
–Foreign matter introduced to brain tissue, possible infection
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Concussions
–Mild, diffuse injury to the brain; effects can last for years
–Typically due to acceleration/deceleration type injury
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Concussion Initial Symptons
Temporary loss of normal function (confusion, disorientation, amnesia),
Loss of consciousness
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Concussion Post Event Symptons
Headache, irritability, lack of concentration, visual disturbances
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Pathophysiology of Primary Injury of TBI
•The tissue damage that occurs at the moment of injury
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Pathophysiology of Secondary Injury of TBI
Complex processes may result:
* Inflammation
* Damage from inflammatory mediators
* Cellular dysfunction
* Cerebral edema
* Increased ICP
* Impaired cerebral perfusion and resulting ischemia and hypoxia
* Brain death/herniation
Also may see complications such as arrhythmias and neurogenic pulmonary edema
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TBI
Diagnostic Interventions-Complete Neurological Exam
Diagnostic imaging
CT: quick and accurate; serial CTs
MRI: more detail; more info on long term outcome
Angiography
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TBI
Diagnostic Interventions-ICU Setting
* ICP monitoring
* Fluid filled vssolid-state systems
* EVD capabilities for therapeutic management
* SjvO2
* Licox
* EEG
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Management- Acute Phase
Manage the Primary Injury
* Transport to a neurotreatment center!
* Manage the primary injury
* Supportive management
* Airway, ventilation, circulation
* Surgery
* Remove masses/hematomas
* Foreign objects/debris
* Debridement of damage tissue
* Perform craniotomy
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Management Acute Phase
Manage Secondary Injury
* Therapeutic hypothermia
* Controlling ICP
* Patient positioning
* Sedation/analgesia, +/- paralytics
* Therapeutic hyperventilation
* Consider vent strategy and ABG goals
* Extra-ventricular Drain (EVP)
* Maintain CPP through ensuring adequate/high MAP
* Fluids and vasopressors if BP too low
* Manage the cerebral edema
* Mannitol
* Lasix
* Hypotonic saline
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TBI Management: Chronic Phase
* Some patients remain in a vegetative state
* Risk of complications (infection, DVT, pressure sores, pneumonia)
* Rehabilitation!
* This may last months to years
* Includes:
* Physiotherapy
* Speech and language therapy
* Cognitive rehabilitation therapy
* Occupational therapy
* Mental health support
* Therapists, psychologists, psychiatrists
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Stroke
–A rupture or blockage of a blood vessel in the brain, depriving parts of the brain of blood supply
–The area of ischemia can become permanently damaged, creating an area of infarct
–Long term effects of stroke depend on the region and size of the area of infarct
–Results in loss of consciousness, paralysis or other symptoms depending on the site and severity of the injury
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Ischemic Stroke
* Thrombotic strokes
* Caused by a blood clot that forms in an artery directly leading to the brain
* Embolic strokes
* Occur when a clot develops somewhere else in the body and travels through the blood stream to the brain
* TIA (Transient Ischemic Attack)
* Caused by a temporary interruption of blood flow to the brain; symptoms are similar to an ischemic stroke except they go away within a few minutes or hours
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Hemorrhagic Strokes
Occur when an artery inside the brain - precipitated by smaller artery bleeds, hypertension and/or a sudden stress
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Predisposing Factors of Stroke
Common cause of death in persons over 65 years of age
Predisposing conditions include:
* Genetics
* Hypertension
* Diabetes
* High cholesterol
* Smoking
* Cardiac disease
* Oral contraceptives
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Sincinnati PreHospital Stroke Scale
* Facial Droop
* One side of the face does not move as well as the other side
* Arm Drift
* When holding both arm straight out one arm will begin it drift down
* Abnormal speech
* slured words, using wrong words, unable to speak
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Meningitis
* Infection of the membranes that surround the brain and spinal cord
* Meningitis is an inflammation the membranes covering the brain and spinal cord:
* Dura mater
* Arachnoid
* Piamater
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Encephalitis
•Inflammation of the brain itself, usually caused by infection
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Myelitis
•Infection of the spinal cord
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Meningitis vs. Encephalitis
These can occur concurrently: e.g. encephalomyelitis
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Encephalitis Etiology
* Any pathogen can invade brain tissue and begin an inflammatory response
* Pathogens:
* Most often viral (people, food/drink, vectors like mosquitos or ticks…e.g. West Nile)
* Many of the current vaccines protect against this (e.g. MMR)
* Herpes simplex virus is the most common cause.
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Encephalitis Pathophysiology
* Inflammation
* Swelling (cerebral edema)
* Can caused increased ICP, abnormal reflexes
* May see:
* Destruction of nerve cells
* Intracerebralhemorrhage
* Brain damage
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Encephalitis Initial Symptons
Initial symptoms are mild
Low-grade fever
Headache, malaise
Clumsiness, unsteadiness, rigidity
Confusion, lethargy, drowsiness
Nausea/vomiting
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Encephalitis As the Disease Progresses
Progressing to more serious as condition worsens
Loss of consciousness, respiratory depression
Muscle weakness/paralysis
Seizures
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Encephalitis Diagnosis
–MRI or CT of head
–Lumbar puncture and CSF exam/culture
–Serology tests to detect virus
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Encephalitis Management
* Supportive care
* Possibly antivirals
* Acyclovir/Zoviraxand foscarnet/Foscavirfor Herpes
* Antibiotics if bacterial etiology
* Corticosteroids for swelling (possibly)
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Meningitis Pathogens
* Viruses, parasites, fungal…
* Bacterial meningitis is rare but deadly
* Pneumococcal, meningiococcalpathogens most common
* Vaccines available
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Meningitis Symptons
Similar to encephalitis but often characterized by
* Sudden fever (bacterial)
* Severe headache
* Stiff neck/stiff back
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Meningitis Diagnosis
–Lumbar puncture and examination/culture of CSF
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Seizures
* Are a symptom of an underlying brain problem
* Result from sudden, abnormal electrical activity in the brain
* Often, but not always, associated with convulsions
* Note: Though often used interchangeably, seizures ≠ convulsions!
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Focal Seizure
•Happen in just one part of the brain
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Generalized Seizure
Happen on both sides of the brain
Can be:
* Grand Mal (generalized tonic-clonic)
* Absence (brief loss of concsiousness)
* Myoclonic (sporadic/isolated jerking movements)
* Clonic(repetitive jerking movements)
* Tonic (muscle stiffness, rigidity)
* Atonic (loss of muscle tone
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Seizure Etiology
NUMEROUS! Some causes include:≠
Those of CNS origin
* Infectious (encephalitis, meningitis)
* Head injuries
* Stroke
* Epilepsy
Those of systemic origin
* Electrolyte imbalances (Na+ particularly)
* Hypoglycemia
* High fever
* Kidney or liver failure
* Illicit drugs
* Withdrawal (ETOH, Benzos, analgesics…)
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Seizure Symptons
Occur suddenly! May include: Convulsions
Or less obvious:
* Blank stare
* Eye movements
* Grunting, snorting
* Sudden falling
* Teeth clenching
* Mood changes
* Tasting a bitter, metallic flavour
* Can last few seconds or up to 15 minutes
Most stop by themselves
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Seizure Warning Signs
* Fear/anxiety
* Nausea
* Vertigo
* Visual symptoms (bright spots, wavy lines…)
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Seizure Management
–Protect the person from injury during the seizure
–Determine the underlying cause
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Seizures are a Medical Emergency When
Seizures are prolonged (more than 5 min)
* Treat with Benzodiazepenesas first line, possibly propofolor barbituates
* Anti-epileptic drugs if recurring
* EEG monitoring done to monitor background activity
The patient doesn’t wake up
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Seizure Supportive Care
•Airway management, ventilation
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Brain Tumors
There are several types of brain tumors. They are generally named for their site or tissue of origin (E.g. Oligodendrogliomas, astrocytomas, medullablastomas, meningiomas…)
Any tumor will have local effects on the surrounding tissue
If the tumor affects the respiratory center, apneas or dysfunction will result. Blood vessel patency can be compromised
Depending on the size of the growth, ICP will rise causing possible compression of brain tissue and subsequent pathology and manifestations
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Spinal Tumors
* Will cause local tissue dysfunction
* Blood vessel compromise and CSF blockage may compound dysfunction
* Any nerve root distal to the tumor will be effected negatively, therefore
* Tumors in the cervical spine can cause complete loss of breathing function
* Tumors in the thoracic spine may effect inter-costal function etc.
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Tumors Clinical Manifestation
Slow growing lesions may be compensated for by the relative shrinking of cerebral ventricles
Clinical manifestations depend on the size and location of the lesion
Possible symptoms include:Headache, nausea and vomiting, mental changes, papilledema, visual disturbances, alterations in sensory and motor function and seizures
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Spinal Cord Injury
Any injury to the nerves of the spinal cord that is caused by trauma instead of disease
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Incomplete Spinal Cord Injury
Damage or dysfunction due to mechanical injury or edema to a part of the cord
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Complete Spinal Cord Injury
Total sensory, motor and autonomic dysfunction distal to the injury
Paraplegia is the result of thoracic/lumbar injury
Quadriplegia is the result of cervical injury
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Spinal Cord Injury and Spinal Nerves
Nerves involved in accessory muscles (sternocleidomastoid, scalene) exit the spine, C1 to C5
Severe damage or severance at C4 or higher will lead to profound respiratory deficit.
Phrenic nerve branches exit the spinal column at C3, C4, and C5
Inter-costal nerves exit the spine from T1 to T 12
Abdominal nerves used in forced exhalation exit the spine, T7 to L1
