Test 4 Flashcards
The brain consists of the ______, _____ & ______
cerebrum, brainstem, and cerebellum
The ____ is composed of the right and left hemispheres
cerebrum
Both hemispheres can be further divided into four major lobes.
Frontal
Temporal
Parietal
Occipital
The ______ lobe controls higher cognitive function, memory retention, voluntary eye movements, voluntary motor movement, and expressive speech in Broca’s area.
frontal
The _____ lobe contains integration of somatic, visual, and auditory data, and Wernicke’s area, which is responsible for receptive speech.
temporal
The _____ lobe is composed of the sensory cortex, controlling and interpreting spatial information
parietal
Processing of sight take place in the _____ lobe.
occipital
The basal ganglia, thalamus, hypothalamus, and limbic system are also located in the ______
cerebrum
The ______ includes the midbrain, pons, and medulla. The vital centres concerned with respiratory, vasomotor, and cardiac function are located in the medulla. The brainstem also contains the centres for sneezing, coughing, hiccupping, gagging, vomiting, sucking, and swallowing
brainstem
Located in the ______ is the reticular formation, which relays sensory information, influences excitatory and inhibitory control of spinal motor neurons, and controls vasomotor and respiratory activity
brainstem
a clear, colourless fluid similar to blood plasma and interstitial fluid. Circulates within the subarachnoid space that surrounds the brain, brainstem, and spinal cord. This fluid provides cushioning for the brain and spinal cord, allows fluid shifts from the cranial cavity to the spinal cavity, and carries nutrients
Cerebro-spinal fluid (CSF)
Peripheral nervous system
Spinal nerves
Cranial nerves
Autonomic nervous system (ANS)
Structures & Functions of Nervous System
Meninges
Skull
Vertebral column
Protective Structures
Central nervous system
Loss of neurons; brain weight decreases; cerebral blood flow decreases; CSF and neurotransmitter release decreases
Peripheral nervous system
Decreased nerve conduction and coordinated neuromuscular activity; intellectual performance remains constant; decreased sensory changes
Age related considerations
Cerebrospinal fluid analysis
Lumbar puncture
Radiological studies
Cerebral angiography
Computed tomography (CT)
Magnetic resonance imaging (MRI)
Positron emission tomography (PET)
Diagnostic Studies of Nervous System
may be done for someone who has NPH, high fever, headache – to check for infection, meningeal irritation
Lumbar puncture
Electroencephalography (EEG)
Electromyography (EMG) and nerve conduction studies
Evoked potentials
Electrographic studies
Carotid duplex studies
Transcranial Doppler ultrasonography
Combined Doppler and ultrasound studies
These tests can determine if there is a nerve problem, muscle problem, demyelination of the nerves.
Vascular system – flow in carotid, not the same blood flow to brain if narrow
Electrographic, Doppler & Ultrasound Studies
Factors that influence _____:
BP
Cardiac function
Intraabdominal pressure
Intrathoracic pressure
Body position
Temperature
Blood gases – especially CO2
Intracranial Pressure (ICP)
Occurs at the initial time of an injury that results in:
displacement,
Bruising
Or damage of the three components.
Primary Injury
Occurs after the primary injury:
Hypoxia
Ischemia
Hypotension
Edema
Increased ICP
Secondary Injury
Total pressure exerted because of the combined total volume of the 3 components of the skull:
Brain Tissue
Blood
CSF
ICP
Above 20mmhg
Life threatening
Occurs with increased brain tissue
Occurs with increased cerebral blood volume
Increased CSF
Any increase can results in hypercapnia, cerebral acidosis, impaired autoregulation, systemic hypertension, cerebral edema.
Increased ICP
An accumulation of fluid in the extravascular spaces of brain tissue
Results in increased tissue volume and possibly increased ICP
Can be caused by lesions, head injuries, brain surgery, cerebral infections, vascular insults and toxic or metabolic encephalopathic conditions
Can be vasogenic, cytotoxic, and interstitial
Cerebral Edema
Change in LOC
Changes in vital signs
Ocular signs
Change in Motor function
Headache
Vomiting
Manifestations of Increased ICP
- _______ intracranial adaptive capacity (related to decreased cerebral perfusion or increased ICP)
- Risk for ineffective cerebral tissue perfusion as evidenced by brain injury, brain neoplasm, cerebral aneurysm
- Risk for disuse syndrome as evidenced by alteration in level of consciousness, mechanical immobility, paralysis
Decreased
Any trauma to the
Skull
Scalp
Brain
Head trauma includes an alteration in consciousness, no matter how brief.
Head Injury
The majority of deaths after a ______ occur immediately after the injury, either from the direct head trauma or from massive hemorrhage and shock.
head injury
Scalp lacerations
Skull fractures
Head trauma
Focal injury (laceration, contusion)
Types of Head Injury
The most minor type of head trauma
Scalp is highly vascular _ profuse bleeding
Major complication is infection
Scalp lacerations
Linear or depressed
Simple, comminuted, or compound
Closed or open
Location of the fracture alters the presentation of manifestations.
Facial paralysis
Battle’s sign
Bilateral periorbital ecchymosis (raccoon eyes)
Rhinorrhea or otorrhea indicates that a fracture has traversed the dura.
Leaking fluid should be tested to determine if the fluid is cerebrospinal fluid (CSF).
Skull fractures
Diffused or localized
Diffuse (Concussion)
A sudden transient mechanical head injury with disruption of neural activity and a change in level of consciousness (LOC)
Brief disruption in LOC
Amnesia
Headache
Short duration
Head trauma
2 weeks to 2 months
Persistent headache
Lethargy
Personality and behaviour changes
Shortened attention span, decreased short-term memory
Changes in intellectual ability
Post-concussion syndrome (head trauma)
Widespread axonal damage following mild, moderate, or severe traumatic brain injury (TBI)
decreased LOC
increased ICP
Decortication, decerebration
Global cerebral edema
Diffuse axonal injury (head trauma)
Lacerations
Contusion
Focal injuries
Involve actual tearing of the brain tissue
Often occur in association with depressed and open fractures and penetrating injuries
Intracerebral hemorrhage is generally associated with cerebral laceration.
Surgical repair of laceration is impossible.
Prognosis is poor with large intracerebral lacerations.
Lacerations (Focal Injury)
Bruising of brain tissue within a focal area that maintains the integrity of the pia mater and arachnoid layers
Coup-contrecoup injury
Prognosis is dependent on the amount of bleeding around the contusion site.
Contusion (Focal Injury)
Results from bleeding between the dura and the inner surface of the skull
Neurological emergency
Venous or arterial origin
Epidural hematoma (complication)
Classic signs
Initial period of unconsciousness
Brief lucid interval followed by decrease in LOC
Headache
Nausea, vomiting
Focal findings
Occurs from bleeding between the dura mater and the arachnoid layer of the meningeal covering of the brain
Usually results from injury to the brain substance and its parenchymal vessels
Usually venous in origin
Much slower to develop into a mass large enough to produce symptoms
May be caused by tearing of small cortical arteries
Epidural hematoma (complication)
Signs within 48 hours of the injury
Similar signs and symptoms to brain tissue compression in increased intracranial pressure (ICP), decreased LOC, and headache
Patient appears drowsy and confused, ranging to unconsciousness
Ipsilateral pupil dilates and becomes fixed
Acute subdural hematoma
Occurs within 2–14 days of the injury
After initial bleeding, a subdural hematoma may appear to enlarge over time.
Subacute subdural hematoma
Develops over weeks or months after a seemingly minor head injury
Peak incidence in 50s and 60s age groups
Chronic subdural hematoma
Occurs from bleeding within the brain tissue
Usually occurs within the frontal and temporal lobes
Size and location of hematoma determine patient outcome
Intraparenchymal Hematoma
Result of traumatic forces damaging the superficial vascular structures that exist in the subarachnoid space
May predispose the patient to cerebral vasospasm and diminished cerebral blood flow (CBF), increasing the risk of ischemic damage following brain injury
Traumatic Subarachnoid Hemorrhage
Treatment principles
Prevent secondary injury
Manage ICP
Timely diagnosis
Surgery if necessary
Craniotomy
Craniectomy
Cranioplasty
Burr-hole approach
Diagnostic Studies and Interprofessional Care
Nursing assessment
Glasgow Coma Scale score
Neurological status
Presence of CSF leak
Nursing Management
Prevent motor vehicle accidents.
Promote wearing of safety helmets and seat belts.
Health promotion - Nursing implementation
Maintain cerebral oxygenation and perfusion.
Prevent secondary cerebral ischemia.
Monitor for changes in neurological status.
Treatment of life-threatening conditions will initially take priority in nursing care.
Major focus of nursing care relates to increased ICP
Eye conditions
Hyperthermia
Raise the head of patients leaking CSF.
Acute intervention - Nursing implementation
Nutrition
Bowel and bladder management
Spasticity
Dysphagia
Deep venous thrombosis
Hydrocephalus
Post-traumatic seizure
Mental and emotional support
Ambulatory and home care - Nursing implementation
Maintain normal cerebral perfusion pressure
Achieve maximal cognitive, motor, and sensory function
Experience no infection or hyperthermia
Achieve pain control
Evaluation - Expected outcomes
Acute inflammation of meningeal tissue
Always arachnoid mater and cerebrospinal infection
Is a medical emergency.
Untreated, the mortality rate is near 100%.
Bacterial meningitis
Increased cerebrospinal fluid (CSF) production
Purulent secretions spread to other areas of the brain through CSF.
If the process extends into the parenchyma, or if concurrent encephalitis is present, cerebral edema and increased intracranial pressure (ICP) become problematic.
Bacterial meningitis
Fever
Severe headache
Nausea, vomiting
Nuchal rigidity
Positive Kernig’s sign
Positive Brudzinski’s sign
Photophobia
↓ Level of consciousness (LOC)
Signs of ↑ ICP
Coma Seizures
Headache
Vomiting
Irritability
Bacterial meningitis
Acute complication is ↑ ICP
Residual neurological dysfunction
The optic nerve (CN II) is compressed by increased ICP.
Ocular movements are affected with irritation to nerves III, IV, and VI.
Irritation of CN VIII causes tinnitus, vertigo, and deafness.
Hemiparesis, dysphagia, and hemianopsia may occur and resolve over time.
Acute cerebral edema
Noncommunicating hydrocephalus if CSF flow obstructed
Waterhouse–Friderichsen syndrome
Bacterial meningitis - Complications
Blood culture
Lumbar puncture and analysis of CSF
X-rays of skull
CT Scan
MRI
Bacterial meningitis - Diagnostics
a group of symptoms caused when the adrenal glands fail to function normally. This occurs as a result of bleeding into the glands. Meningococcemia is a life-threatening infection that occurs when the bacteria Neisseria meningitidis invades the blood stream. – whole vascular system can collapse within the brain
Waterhouse-Friderichsen syndrome (WFS)
Rapid Diagnosis based on history and physical exam
Antibiotic therapy instituted after collection of specimens
Interprofessional Care
Neurological evaluation
Vital signs
Assessment of fluid intake and output
Evaluation of the lungs and skin
Nursing Assessment
Inadequate intracranial adaptative capacity
Hyperthermia
Potential for inadequate cerebral tissue perfusion
Acute pain
Bacterial Meningitis: Nursing Diagnoses
Patient will
Have minimal disorientation
Lack evidence of agitation
Have satisfactory pain relief
Participate in treatment
Have normal body temperature
Bacterial Meningitis: Evaluation
Most common causes are enterovirus, arbovirus, HIV, and herpes simplex virus (HSV)
Usually presents as a headache, fever, photophobia, and stiff neck
Diagnostic testing of CSF
Polymerase chain reaction (PCR) to detect viral-specific DNA/RNA
Symptomatic management with full recovery expected
Viral Meningitis
Acute inflammation of the brain
Sometimes fatal
Caused by viruses
Ticks or mosquits can transmit epidemic encephalitis
Cytomegalovirus (CMV) encephalitis is common in patients with AIDS
Encephalitis
Nonspecific
- Fever
- Headache
- Nausea, vomiting
Incubation period 3–14 days
Signs appear on day 2 or 4
- May vary from minimal alterations to coma
Hemiparesis
Tremors
Seizures
Cranial nerve palsies
Hemiparesis
Tremors
Seizures
Cranial nerve palsies
Encephalitis:Clinical Manifestations
CT
MRI
PET
PCR test for HSV DNA/RNA
Blood test for West Nile viral RNA
Encephalitis:Diagnostic Studies
Mosquito control for prevention
Acyclovir (Zovirax), ganciclovir (Cytovene) for HSV infection (start before onset of coma)
Antiseizure medications for seizures
Encephalitis: Nursing and Interprofessional Management
Accumulation of push within brain tissue
Streptococci and Staphylococcus aureus are causative organisms
Headache
Fever
Nausea, vomiting
Signs of increased ICP
Symptoms reflect local area of abcess
Brain Abscess
Primary – arising from tissues within the brain
Secondary – from metastasis
Brain tumour
Commonly classified as peripheral neuropathies
Disorders usually involve motor, sensory, or both
Causes include:
Tumours
Trauma
Infections
Inflammatory processes
Unknown causes
Cranial nerve disorders
Average age of onset is 60
Rarely diagnosed in people less than 40
Women more often than men
Pathophysiology not fully understood
Trigeminal Neuralgia
Abrupt onset of:
Paroxysms of flashing
Stabbing pain
Attacks are usually brief
Usually initiated by a triggering mechanism
Chewing
Brushing teeth
Hot/cold air
Trigeminal Neuralgia
Anticonvulsive medications – Tegretol
First line of treatment
Acts on sodium channels to lengthen neuron repolarization and therefore decreased neuron firing.
S/E - Blood abnormalities from bone marrow suppression
Antispasmodics – Baclofen
Can be given with the anticonvulsant medication or on its own
Reduces pain
Other anticonvulsants – gabapentin
OTHER TREATMENT
Analgesic blocks – pain relief for 6 – 18 months
Biofeedback
surgery
Trigeminal Neuralgia - Drug Therapy
Disorder characterized by disruption of the motor branches of CN VII
One side of the face
Absence of other disease such as stroke
Exact etiology unknown
Immune
Infective ischemic mechanisms
Acute onset
Unilateral facial paralysis affecting muscles of the upper and lower face
Diagnosis is based on clinical presentation.
Corticosteroid treatment
Bell’s Palsy
Acute, rapidly progressing polyneuritis
Manifests as symmetrical ascending paralysis from the results in loss of myelin, inflammation and edema of the affected nerves.
Etiology is unknown but thought to result from an immunological reaction.
EMG and nerve conduction studies show evidence of demyelination.
Lumbar Puncture may show elevated protein 10 days after the onset of symptoms.
Guillain-Barre Syndrome
Acute phase – patient is in the ICU
Patient is at risk for:
- Respiratory problems and infection.
Anxiety
Nutritional deficiencies
Skin breakdown
Pain management
Communication difficulties
Fluid and electrolyte disturbances
Recovery phase - involves intense long term rehabilitation.
Guillain-Barre Syndrome
An acute neurological disorder that causes life threatening neuroparalysis
From a spore forming bacterium – clostridium botulinum, that produces a neurotoxin
The toxin destroys or inhibits the neurotransmission of acetylcholine at the myoneural junction
A reportable disease
Symmetrical descending motor paralysis no sensory deficits
Treatment IV botulinum antitoxin
Gastric lavage, laxatives, to decrease the absorption of toxin – must not have magnesium because it worsens toxin induced neuro muscular blockade.
BOTULISM
inflammation of the nerve roots and polyneuritis occurs from a neurotoxin produced by clostridium tetani.
Spores are present in the soil, garden mould and manure
Enters the body through a wound
Incubation period 3 - 21 days
Stiffness in the jaw or neck; symptoms of infection like fever, malaise,
Progresses to other areas causing increased rigidity
If progresses, then opisthotonos (extreme arching of the back and retraction of the head) during convulsion
Symptoms of an over stimulated sympathetic nervous system – diaphoresis, labile hypertension, tachycardia, hyperthermia, dysrhythmias.
Seizures with slight stimulation like lights, motions noise.
Managed with tetanus and diphtheria toxoid booster and tetanus immune globulin
Tetanus
Caused by treponema pallidum organism which invades the central nervous system
Fatal if not treated.
Can occur at any time during the course of syphilis
Late symptoms include degenerative changes in the spinal cord (tabes dorsalis) and the brain stem (general paresis).
Charcot joints - enlarged hypermobile joints with bone destruction
Seizures, vision and hearing impairment
Neurological and psychiatric symptoms
Penicillin, symptomatic care
Neurosyphilis
Can have a devastating effect on health and well-being
SCI is divided into traumatic (result of external physical impact) and non-traumatic (result of disease, infection, or tumour) categories
Spinal Cord Injuries
Primary injury (initial injury) to the spinal cord.
Cord compression
Initial injury disrupts axons, blood vessels and cell membranes
Etiology and Pathophysiology- Spinal Cord Injury
Secondary injury
Ongoing, progressive damage that occurs after initial injury
Apoptosis may occur weeks to months after the initial injury
Ischemia, hypoxia, microhemorrhage and edema.
Etiology and Pathophysiology- Spinal Cord Injury
Temporary neurological syndrome
Characterized by
Decreased reflexes
Loss of sensation
Flaccid paralysis below level of injury
Experienced by about 50% of people with acute spinal cord injury
Spinal shock
Loss of vasomotor tone caused by injury
Characterized by hypotension, hypothermia, and bradycardia (important clinical cues)
Loss of sympathetic nervous system innervation causes
Peripheral vasodilation
Venous pooling
Decreased cardiac output
Neurogenic shock
Classified by mechanism of
Injury
Most are related to flexion, hyperextension, flexion rotation, extension-rotation and compression
Skeletal level of injury
Neurological level of injury
Completeness or degree of injury
Spinal and Neurogenic ShockClassification of Spinal Cord Injury
Skeletal injury at the vertebral level
Tetraplegia or paraplegia
Neurological level is the lowest where sensory and motor function are both normal
Level of Injury
Damage to central spinal cord either complete or incomplete
Motor weakness and sensory loss are present in both upper and lower extremities.
6 syndromes
Central cord syndrome
Anterior cord syndrome
Brown-Sequard
Posterior cord syndrome
Cauda equina syndrome
Conus medullaris syndrome
Degree of InjuryCentral Cord Syndrome
motor problems, temperature problems – below the injury, touch remains in tact (position, vibration & motion)
Anterior cord syndrome
remain in tact with anterior idk what she said that was fucked
Posterior tract
Results from cord compression, ischemia, edema , cord transection (rare)
Symptoms are related to the level and degree of the injury
The higher the injury the more serious
Combined motor and sensory symptoms
Clinical Manifestations - Spinal Cord Injury
Respiratory
- total loss of respiratory muscle function above level of C4
Cardiovascular
- bradycardia
Urinary System
- retention
Gi System
- injury above T5 leads to gastric hypomotility
Integumentary
- high risk of skin breakdown
Metabolic
- loss of body weight
- high nutritional needs
Thermoregulation
- poikilothermic
Peripheral Vascular
- DVT, PE
Clinical Manifestations - Spinal Cord Injury
CT scan may be used to assess stability of injury, location, and degree of bone injury.
MRI is gold standard for imaging neurological tissues.
Comprehensive neurological examination
Assessment of head, chest, abd for additional injuries or trauma
Vertebral angiography if there is altered mental status – to rule out vertebral artery damage.
Diagnostic studies
