Title: Patient with Neurologic Problems
1Patient with Neurologic Problems
2Rapid Neurologic Assessment
- Glasgow Coma Scale
- Response to painful stimulisternal rub,
trapezius squeeze - Level of consciousnesseven a subtle change is
the first indicator of a decline in neurologic
status - Decorticationabnormal posturing seen in the
client with lesions that interrupt the
corticospinal pathways. The patients arms,
wrists, and fingers are flexed with internal
rotation and plantar flexion of the legs.
3Rapid Neurologic Assessment cont.
- Decerebration-abnormal posturing and rigidity
characterized by extension of the arms and
legs,pronation of the arms, plantar flexion and
opisthotonos (kind of spasm with head and feet
bent backward and body bowed forward). Indicates
dysfunction of the brainstem.
4Rapid Neurologic Assessment cont.
- Pupillary assessment, mental exam
- Cranial nerve exam
- Olfactory
- Optic
- Oculomotor
- Trochlear
- Trigeminal
- Abducens
- Facial
- Acoustic
- Glossopharyngeal
- Vagus
- Spinal accessory
- hypoglossal
5Brain DisordersMigraines
- Caused by a phenomenon called cortical spreading
depression whereby neurological activity is
depressed over a specific area of the
cortexformerly felt to be related to dilation of
cerebral blood vessels - Results in release of inflammatory mediators
leading to irritation of the nerve roots,
especially the trigeminal nerve - Serotonin release involved in the causation
- Diagnosis is based on HP, neurologic exam and
imaging.
6Migraines
- Triggers
- Tyramine-containing food and beverages such as
beer, wine, aged cheeses, chocolate, yeast, MSG,
nitrates, artificial sweeteners, smoked fish - Medicationsestrogens, nitroglycerine,
nifedipine, cimetidine - Other fatigue, hormonal fluctuations, missed
meals, sleeping problems, varying altitudes
7Commonly Used Drugs for Migraines
- NSAIDs
- Beta blockers such as inderal
- Calcium channel blockers-verapamil
- Abortive drugs such as ASA, acetaminophen
- Ergotamine preparations
- Triptans
- Opioids
- Investigationaldroperidol (Inapsine)
8Seizures
- Abnormal, sudden, excessive, uncontrolled
electrical discharge of neurons within the brain.
May cause change in LOC, motor or sensory
ability, and/or behavior. - Epilepsychronic disorder characterized by
recurrent, unprovoked seizure activity
9Types of Seizures
- Generalized
- Absencepetit mal
- Tonic-clonicgrand mal. Muscle stiffening
followed by jerking - Myocloniccontractions of body muscles
- Atonicgo limp, drop attacks
- Partialsimple partial, complex partial
- others
10Antiepileptic Drugs
- Tegretolpartial or generalized seizures
- Klonopinabsence, myoclonic and akinetic seizures
- Valiumstatus epilepticus
- Depakoteall types
- Zarontin-absence seizures
- Neurontinpartial seizures
- Dilantin-all types
- Topamaxfor intractable partial seizures
- Keppraadjunct in partial seizures
11Common side effects of anti-epileptics (AEDs)
- Teratogenic potential
- Medication interactions
- Blood dyscrasias
- Altered liver function
- Effects on renal function
- Wt. gain or loss
- Sometimes sedation
12Surgical options
- Identify seizure area by EEG, insert electrodes,
surgically excise - corpuscallostomy
13Characteristics of Seizures
- Important to observe and document
- How often?
- Description
- Progression
- Duration
- Last time occurred
- Preceded by aura?
- What does patient do post-seizure?
- Time elapsed before returns to baseline
14Seizure Precautions
- Stay with patient
- O2
- Airway
- Suction
- IV access
- Siderails up, padded
- Bed in lowest position
- Turn patient to side
- Loosen restrictive clothing
- Do not force anything into the mouth
- Following seizuredo neuro checks
15Status Epilepticus
- Characterized by prolonged seizures lasting more
than 5 minutes or repeated seizures over the
course of 30 minutes - Is a medical emergency. Brain damage and death
can ensue. - Untreated can cause hypoxia, hypotension,
hypoglycemia, dysrhythmias and lactic acidosis.
Rhabdomyolysis can occur with effects on the
kidneys.
16Treatment of Status Epilepticus
- Lorazepam is the drug of choice due to rapid
onset of action and long duration of action - Valium
- Phenobarbital
- Dilantin
- Supportive/safety care
17Meningitis
- Inflammation of the meninges or brain covering
- Entry is via the bloodstream at the blood-brain
barrier. May be direct route or via skull
fracture. Exudate will develop. - Viral is most common
- Fungal-Cryptococcal. Can be caused by sinusitis
- Bacterial-mortality rate25. Most commonly
caused by Neisseria meningitidis and
Streptococcus pneumoniae.
18MeningitisS/S
- LOC
- Disorientation
- Photophobia
- Nystagmus
- hemiparesis
- CN dysfunction
- Personality changes
- N/V
- Fever and chills
- Red macular rash
- Nuchal rigidity, positive Kernigs (hamstring
pain w/extension) and Brudzinskis (flexion of
the hips when the neck is flexed)
19Review of CSF findings
- Pressure lt20cm of H2O
- Clear, colorless. Cloudy indicates infection.
Pink to orangeRBCs - Cells 0-5 lymphocytes normal.
- Glucose50-75mg/dL normal, less than 50 indicates
infection - Proteins 15-45 normal, 45-100 paraventricular
tumor, 50-200 viral, more than 500bacterial
infection
20Meningitis cont.
- CSF findings
- Bacterialcloudy, increased WBCs, increased
protein, decreased glucose, elevated CSF pressure
gt180mm h20 - Viralclear, increased WBCs, slighly elevated
protein, normal glucose, variable CSF pressure
21Meningitis
- May display s/s of increased ICP ( see following
slide) - Left untreated, can result in brain herniation or
damage
22Meningitis
- Treatment according to causative pathogen as
found by LP (lumbar puncture) - Bedrest
- IV fluids, analgesics for pain and fever
- Anticonvulsants
- Corticosteroids
- Pathogen specific abxmeningococcus penicillin or
cephalosporins, contacts rifampin or cipro
pneumococcalPCN, cephalosporins and also
vancomycin
23 ICP
- Pressure-volume relationship between ICP, volume
of CSF, blood, brain tissue and cerebral
perfusion pressure (Monroe-Kellie Hypothesis) - Cranial compartment is incompressible and cranial
contents should have a fixed volume - Equilibrium must be maintained. Increased volume
will result in downward displacement of the brain
24Key Features of Increased Intracranial Pressure
- Lethargy to coma
- Behavioral changes
- Headache
- N/V
- Change in speech pattern
- Aphasia
- Pupillary changes--papilledema
- Cranial nerve dysfunction
- Seizures
- Abnormal posturing
- Cushings Triadelevated BP, decreased pulse and
decreased respirations
25Treatment of increased ICP
- Maintain airway
- Hyperventilate patient to blow off CO2 (CO2
dilates blood vessels) - Raise HOB to allow for venous drainage
- Decrease metabolic demands by paralyzing and
sedating patient - Mannitol
- corticosteroids
- Pain management
- Intracranial monitoring (in ventricle)
- Craniotomies
- Decompressive craniectomy
26Brain Attacks (Strokes or CVAs)
- Affects over 550, 000 Americans per year
- Two major typesischemic and hemorrhagic
- Caused by disruption of the normal blood supply
to the brain - May be preventable if causes discovered early
27Risk Factors for Brain Attacks
- Obesity
- Heart disease
- Diabetes mellitus
- Hypercholesterolemia
- Hypercoagulable states
- Cocaine, illicit drug use
- Atrial fibrillation
28Differential Features of the Types of Stroke
- Thromboticonset is gradual
- Usually related to ASHD and hypertension
- Intact LOC
- May have speech and visual changes
- Slight HA
- No seizures
- Deficits may be permanent
29Differential of strokes
- Embolic
- Abrupt
- Steady progression
- Awake
- May be associated with cardiac disease
- Maximal deficits at onset
- No seizures
- Rapid improvements
30Differentials of strokes
- Hemorrhagic
- Sudden onset
- Deepening stupor or coma
- May have hypertension
- Focal deficits
- Seizures possible
- Permanent deficits possible
- May result from an aneurysm, rupture of an AV
malformation or severe hypertension
31Ishemic Stroke
- Caused by a blockage of a blood vessel
- Generally caused by atherosclerosis
- Early warning signs include transient loss of
vision, transient ischemic attack (called silent
strokes) - Risk factors atrial fibrillation, ASHD, cocaine
use/abuse, hx of blood clots - Treatmentclot buster TPA, streptokinase,others
32Transient ischemic attack vs. reversible ischemic
neurologic deficit
- Ischemic strokes are often preceded by warning
signs such as TIAs or RINDs - Both cause transient focal neurologic dysfunction
from a brief interruption in cerebral blood flow - TIAs last minutes to lt24h
- RINDs last gt24h but less than a week
33Hemorrhagic strokes
- If survive event, recovery from hemorrhagic
stroke better than ischemic - Caused by vascular disruption e.g. aneurysms, AVM
- Surgical decompression
34Assessment of patient with brain attack
- Neurologic exam
- Motor examhemiplegia vs. hemiparesis
- Sensory changes-neglect syndrome (most notable in
right cerebral hemispheric injuries) - Amaurosis fugaxtemporary loss of vision in one
eye - Hemianopsiablindness in one half of visual field
- Cranial nerve function
- Cardiovascular assessmentabrupt reduction of BP
not advised
35Assessment
- Baseline CT, MRI even better (want to ensure that
the stroke is not hemorrhagic) - ECG
- Echocardiogram
- Cardiac enzymes
36Interventions
- Depending of type of brain attack
- Anticoagulants (assuming not a bleed)
- Catheter directed thrombolytic therapymay use if
systemic tx not effective - Endarterectomy
- Craniotomy
- Systemic thrombolytic txmust meet strict
criteria. Must give within 3hours of onset of s/s - Wire coils in aneurysmsseals the area
37Key considerations
- Impaired physical mobility self care deficit
- Disturbed sensory perception
- Unilateral neglectin rt cerebral stroke. May
have lack of proprioception and failure to
recognize their impairment - Impaired verbal communicationexpressive aphasia
(Brocas), receptive aphasia (Wernickes)
38Parkinsons disease
- Genetic and environmental contributors
- Associated with four cardinal s/s tremor,
rigidity, akinesia (slow movements), and postural
instability - Degeneration of substantia nigradecreased
dopamine. Acetylcholine will predominate. Also
with norepinephrine loss thus the postural
hypotension.
39Parkinsons Key Features
- Stooped posture
- Slow and shuffling gait
- Pill-rolling, mask-like facies, uncontrolled
drooling, rare arm swinging with walking - Change in voice, dysarthria and echolalia
- Labile and depressed, sleep disturbances
- Oily skin, excessive perspiration, orthostatic
hypotension
40Parkinsons Disease
- Stages
- Initial-hand and arm trembling, weakness,
unilateral involvement - Mild-masklike facies, shuffling, bilateral
involvement - Moderateincreased gait disturbances
- Severeakinesia, rigidity
- Complete dependence
41Interventions
- Eldepryl (MAO inhibitor which decreases the
breakdown of dopamine) - Dopamine agonistsstimulate dopamine receptors
but have side effects such as nausea, drowsiness,
postural hypotension and hallucinations. Mirapex
and Requip mimic the actions of dopamine.
42Interventions cont.
- Levodopa/carbidopa. Used as disease progresses.
Wearing off phenomenon. - Amantadineused to treat the wearing off s/s.
- Stavelo(carbidopa/levodopa/entacapone).
Dopa-decarboxylase inhibitor/dopamine
precursor/COMT inhibitor. Useful in end-stage
disease.
43Drug toxicity/tolerance in PD
- Reduce medication dosage
- Change of medications or in the frequency of
administration - Drug holiday up to 10 days
44Nursing considerations
- Maintain mobility and flexibility by ROM
- Encourage self-care as much as possible
- Monitor sleep patterns to avoid injury
- Nutrition-may need soft or thickened foods.
- Constipation
- Speech therapy may be needed
- Psychosocial supportimpaired memory cognition
45Surgical Management in PD
- Stereotactic pallidotomy
- Deep brain stimulation when meds no longer work.
Electrode is implanted and connected to a
pacemaker in chest. - Fetal tissue transplantation using fetal
substantia nigra (implanted in the caudate
nucleus of the brain).
46Alzheimers Disease
- Chronic progressive degenerative disease usually
seen in individuals older than 65 - Characterized by loss of memory, judgment, and
visuospatial perception and by a change in
personality - Progressively physically and cognitively impaired
resulting ultimately in death
47AD
- Increased amount of beta amyloid
- Neurofibrillary tangles throughout the neurons
- Neuritic plaques
- Granulovascular degeneration
- Reduced levels of acetylcholine
- ? Increased levels of glutamate
48Key Features of AD
- Early-forgets names, misplaces household items,
mild memory loss, short attention span, subtle
changes in personality, wanders, impaired
judgment - Middlecognition vitally impaired disoriented to
time, place and event agitated unable to care
for self, incontinent - Severe-incapacitated motor and verbal skills lost
49Physical Assessment of AD
- Observe for stage of progression
- Observe for changes in cognitionattention,
judgment, learning and memory, communication/langu
age - Observe for changes in behavior
- Changes in self-care skills
- Psychosocial assessment
- Dx of exclusion. Check CMP, CBC, B12, folate,
TSH, RPR, drug toxicities and levels, alcohol
screening - PET or MRI to r/o pathology
50- Mini-mental state examinationorientation,
registration (repeat three words), naming,
reading and following directions. - Good one is to have them draw a clock with an
indicated time
51Interventions for AD
- Provide environmental stimulation through contact
with people, provide a clock and calendar,
present change gradually, allow for rest periods,
use repetition - Be concrete
- Limit information
- Prevent overstimulation and provide structure
52Interventions cont.
- Promote independence in ADL
- Be consistent
- Promote bowel and bladder contenence fy offering
rest room breaks q2h daytime, limit fluids at hs - Administer cholinesterase inhibitors such as
Aricept, Reminyl and Exelon. Maintains
functionality for a few more months.
53Interventions cont.
- Provide ID band
- Monitor to ensure safety from wandering
- Walk patient to reduce restlessness
- Involve in activities
- Restraints only as last resort
54Multiple Sclerosis (MS)
- Also called disseminated sclerosis or
encephalomyelitis disseminata - Chronic, inflammatory disease of CNS
- Causes gradual destruction of myelin sheath of
neurons. Results in scars or sclerosis on the
myelin sheaths. - Results from autoimmune process
- Between attacks, s/s may resolve but permanent
injury occurs as disease progresses
55MS
- Usually affects adults 20-40 years of age
- More common in women than men
- Occurs in more temperate climates
- No cure
56MS signs and symptoms
- Changes in sensation
- Muscle weakness
- Incoordination, loss of balance
- Dysarthria
- Dysphagia
- Visual problems (diplopia)
- Fatigue
- Bladder and bowel problems
- Cognitive impairment
- Heat intolerance
- indicates initial or presenting symptoms
57Diagnosis of MS
- MRI
- CSF testing will show oligoclonal bands
- Visual evoked potentials and somatosensory evoked
potentials (sensory and visual nerves respond
less actively in MS) - Antibody testing for myelin oligodendrocyte
glycoprotein and myelin basic proteinin
formative stages for testing at this time
58Types
- Relapsing-remitting--charac. by remissions and
relapses - Secondary progressive
- Primary progressiveno remissions, gradual
decline - Progressive relapsingsteady decline with
superimposed attacks
59- ---Copaxone (immunomodulator that targets
T-cells, decreases inflammation), Avonex
(interferon beta), Betaseron (interferon beta),
Tysabri (immunotherapy) - Avoidance of over-heating (Uththoffs phenomenon)
60Spinal Cord Injury
- Force applied to spinal cord will result in
neurologic deficits - Injury may be direct insult to the spinal cord or
may be secondary to a contusion, compression or
to a concussion (loss of function resulting from
a blow)
61Primary mechanisms of injury
- Hyperflexion injury occurs when the head is
suddenly and forcefully accelerated forward,
causing extreme flexion of the neck. Often occurs
in head-on collisions and diving accidents
62Primary mechanisms of Injury
- Hyperextension injuries occur most often in
automobile accidents in which the clients
vehicle is struck from behind or during falls
when the clients chin is struck. The head is
accelerated and decelerated. Results in
stretching or tearing longitudinal ligament,
fractures or subluxates vertebrae and may rupture
the disc.
63Primary mechanisms of injury cont.
- Axial loading (vertical compression) occurs from
diving accidents, falls on the buttocks, or a
jump in which a person landed on their feet. The
blow may cause the vertebrae to shatter. Pieves
of bone enter the spinal canal and damage the
cord.
64Secondary Injury
- Neurogenic shock
- Vascular insult
- Hemorrhage
- Ischemia
- Fluid and electrolyte imbalance
65Extent of Injury
- Most spinal cord injuries are incomplete lesions
- Specific syndrome result from incomplete lesions
66Cervical Injuries
- May produce
- Anterior cord syndrome
- Posterior cord syndrome
- Brown-Sequard syndrome
- Central cord syndrome
- Cauda equina syndromes are associated with
injuries to the lumbar and sacral cord
67Cervical Injuries
- Anterior cord syndrome results from damage to the
anterior portion of both gray and white matter of
the spinal cord, generally 2ndary to decreased
blood supply. Motor function, pain and
temperature sensation are lost below the level of
injury but touch, position and vibration remain
intact.
68- Posterior cord lesionrare. Results from damage
to the posterior gray and white matter of the
spinal cord. Motor function remains intact but
the patient loses the sense of position
sensation, of crude touch and of vibration.
69- Brown-Sequardresults from a penetrating injury
that causes hemisection of the spinal cord or
injuries that affect half of the spinal cord.
Motor function, proprioception, vibration and
deep touch sensations are lost on the same side
of the body as the lesion. On the opposite of the
lesion, the sensations of pain, temperature and
light touch are affected.
70- Central cord syndromeresults from a lesion of
the central portion of the sc. Loss of motor
function is more pronounced in the upper
extremities than in the lower extremities.
Sensation varies.
71- Lumbosacral Injuriesdamage to the cauda equina
or conus medullaris produces a variable pattern
of motor or sensory loss as the peripheral nerves
have the potential for recovery and regrowth.
This injury generally results in a neurogenic
bowel and bladder.
72Vital statistics of spinal cord injuries
- Primary cause is trauma secondary to MVA
- Unmarried male between 16-30
- Generally are Causcasian
- Most injuries are cervical
73Assessment
- Thorough history including mechanism of injury,
any changes since initial responder, previous
medical history, hx of osteoporosis,
osteomyelitis or previous neck or back injuries
or surgeries
74Assessment
- First priority for the client with a SCI is
assessment of the respiratory pattern and airway - Ensure neck is stabilized
- Assess for evidence of abdominal hemorrhage or
other sites of injury/hemorrhage - Glasgow Coma Scale
- Detailed assessment of the clients motor and
sensory status
75Spinal Shock
- Occurs immediately after injury as a result of
disruption of pathways between upper motor
neurons (lie in cerebral cortex) and lower motor
neurons (lie in spinal cord). - Characterized by
- Flaccid paralysis
- Loss of reflex activity below level of lesion
- Bradycardia
- Possible paralytic ileus
- Hypotension.
- May last days to weeks reversal indicated by
return of reflex activity
76Assessment
- Sensory function
- C4-5 can shrug
- C5-6 can pull up arms against resistance
- C7 can overcome resistance with arms flexed
- C8 can grasp objects
- L2-4 can raise legs straight up against
resistance - L5 apply resistance when patient dorsiflexes
- S1apply resistance while the client plantar
flexes his feet
77Cardiovascular
- Dysfunction r/t disruption of the autonomic
nervous system, especially if above T-6 - Bradycardia, hypotension and hypothermia may
result from disruption of sympathetic input - BP lt 90 torr requires intervention to ensure
satisfactory perfusion of the spinal ccord
78Respiratory
- Can develop from both immobility and from
interruption of spinal innervation to the
respiratory muscles - C3-5 innervate the diaphragm
79Gastrointestinal and Genitourinary assessment
- Must assess the patients abdomen for indications
of hemorrhage, distention or paralytic ileus - Ileus may develop within 72h of the injury. Can
cause areflexic bladder which can lead to urinary
retention and a neurogenic bladder.
80Musculoskeletal Assessment
- Assess muscle tone and size
- Muscle wasting is 2ndary to long-term flaccid
paralysis seen in lower motor neuron lesions
(cell body lies in ant. gray column of spinal
cord. Innervates striated muscles). - Upper motor neuron lesions (neuron body lies in
cortex, axon synapses with lower motor neuron).
Causes spasticity.
81Interventions for Patients with Spinal Cord
Injuries
- Immobilization for cervical injuriesfixed
skeletal traction such as halo fixation or tongs - Maintain proper alignment of head, neck and body
- Turn using the log roll technique
- Monitor skin integrity
- Traction pin insertion site care
- If thoracic or lumbosacral injuryimmobilize with
corset or brace - Medicationssupportive, may use steroids,
baclofen, other meds under investigation
82Interventions for patients with SCIs
- Surgical decompression and stabilizationspinal
fusion, insertion of Harrington rods, laminectomy
(excision of a posterior vertebral arch) - Prevent complications of immobility
- Promote self-care
- Bladder retrainingspastic (UMN) or flaccid (LMN)
may be able to initiate voiding or may need IO
catherterizations
83Interventions cont.
- Bowel retrainingLMN may have to have manual
disimpactions, see p. 993. - Rehab, involve community resources
- Home care management
- Psychosocial implications
84Autonomic Dysreflexia or Hyperreflexia
- Commonly seen in patients with injury to the
upper spinal cord (T5 and above). Caused by
massive sympathetic discharge of stimuli from the
autonomic nervous system. - Stimulus sends nerve impulses to sc, travel
upward until blocked by lesion at level of
injury. Cant reach brain so reflex is activated
that increases activity of sympaathetic portion
of ANS.
85Autonomic dysreflexia cont.
- Increased activity of sympathetic portion of ANS
results in spasms and a narrowing of blood
vessels with resultant rise in BP. Brain
perceives elevated BP, sends message to heart
which slows down and dilates vessels above level
of injury to dilate. Brain cannot send messages
below level of injury so BP cannot be regulated.
86Autonomic Dysreflexia
- Precipitated by distension of the bladder or
colon catheterization of or irrigation of the
bladder - Is a medical emergency
87Key Features of Autonomic Dysreflexia
- Sudden onset of severe, throbbing headache
- Severe, rapidly occurring hypertension
- Bradycardia
- Flushing above the level of the lesion
- Pale extremities below the lesion
- Nausea
- Blurred vision
- Piloerection
- Feeling of apprehension
88Care of Patient experiencing Autonomic Dysreflexia
- Place in sitting position
- Notify physician
- Loosen tight clothing
- Assess for cause
- Check foley cath
- If no cath, check bladder for distention
- Place anesthetic ointment on tip of catheter
before insertion
89Care of Patient with Autonomic Dysreflexia cont.
- Check for fecal impaction, disimpact with
anesthetic ointment if present - Check room to ensure not too cool
- Monitor BP q15 minutes
- Give nitrates or hydralazine as ordered
90Myasthenia Gravis (MG)
- Autoimmune disease of neuromuscular junction.
Characterized by flare-ups and remissions. Caused
by auto antibody attack on the acetylcholine
receptors. May be related to hyperplasia of the
thymus. - Presents with muscle weakness that improves with
rest, poor posture, ocular palsies, ptosis,
diplopia, respiratory compromise, bowel and
bladder problems
91MG
- Diagnosis based on HP, labs which include
thyroid studies, tests to R/O inflammatory
illnesses, (RA, SLE, polymyositis), acetylcholine
receptor antibodies (positive confirms but
negative does not rule out)
92MG
- Testing with cholinesterase inhibitors
(Tensilon). Baseline muscle strength tested then
injection given. Within 30-40 seconds, most
myasthenic patients show a marked improvement in
muscle tone that lasts several minutes. - May be used to distinguish between myasthenic
crisis and cholinergic crisis.
93Myasthenic Crisis
- Undermedicated with anticholinesterase drugs.
- Increased pulse and respirations
- Rise in BP
- Anoxia
- Cyanosis
- Bowel and bladder incontinence
- Absence of cough and swallowing reflex
94Cholinergic crisis
- Like being tx with chemical weapons
- Too much acetylcholine
- Nausea, vomiting, diarrhea
- Abdominal cramps
- Muscle twitching
- Hypotension
- Blurred vision
95Treatment of MG
- Immunosuppression with steroids, Imuran or
Cytoxan - Plasmapheresis
- Resp. support
- Nutritional support
- Eye protection if unable to close eyes completely
- Thymectomy
- Maintanancecholinesterase inhibitor drugs such
as Mestinon