This document provides an overview of rapid neurologic assessment techniques including the Glasgow Coma Scale and assessment of level of consciousness. It also discusses conditions such as migraines, seizures, meningitis, increased intracranial pressure, strokes, Parkinson's disease, and Alzheimer's disease. For each condition, it outlines signs and symptoms, diagnostic testing, treatment options, nursing considerations, and interventions.
Stroke or Cerebrovascular incident, is defined as an abrupt onset of a neurological deficit that is attributable to a focal vascular cause.
The clinical manifestations of stroke are highly variable because of the complex anatomy of the brain
Stroke or Cerebrovascular incident, is defined as an abrupt onset of a neurological deficit that is attributable to a focal vascular cause.
The clinical manifestations of stroke are highly variable because of the complex anatomy of the brain
Edward Fohrman | Anesthetic Considerations for Intracranial TumorsEdward Fohrman
Read Edward Fohrman's thoughts on Anesthetic considerations for intracranial tumors. Edward is the Founder and CEO of Fohrman Anesthesia.
Read more at EdwardFohrman.com
Edward Fohrman | Anesthetic Considerations for Intracranial TumorsEdward Fohrman
Read Edward Fohrman's thoughts on Anesthetic considerations for intracranial tumors. Edward is the Founder and CEO of Fohrman Anesthesia.
Read more at EdwardFohrman.com
Deep Behavioral Phenotyping in Systems Neuroscience for Functional Atlasing a...Ana Luísa Pinho
Functional Magnetic Resonance Imaging (fMRI) provides means to characterize brain activations in response to behavior. However, cognitive neuroscience has been limited to group-level effects referring to the performance of specific tasks. To obtain the functional profile of elementary cognitive mechanisms, the combination of brain responses to many tasks is required. Yet, to date, both structural atlases and parcellation-based activations do not fully account for cognitive function and still present several limitations. Further, they do not adapt overall to individual characteristics. In this talk, I will give an account of deep-behavioral phenotyping strategies, namely data-driven methods in large task-fMRI datasets, to optimize functional brain-data collection and improve inference of effects-of-interest related to mental processes. Key to this approach is the employment of fast multi-functional paradigms rich on features that can be well parametrized and, consequently, facilitate the creation of psycho-physiological constructs to be modelled with imaging data. Particular emphasis will be given to music stimuli when studying high-order cognitive mechanisms, due to their ecological nature and quality to enable complex behavior compounded by discrete entities. I will also discuss how deep-behavioral phenotyping and individualized models applied to neuroimaging data can better account for the subject-specific organization of domain-general cognitive systems in the human brain. Finally, the accumulation of functional brain signatures brings the possibility to clarify relationships among tasks and create a univocal link between brain systems and mental functions through: (1) the development of ontologies proposing an organization of cognitive processes; and (2) brain-network taxonomies describing functional specialization. To this end, tools to improve commensurability in cognitive science are necessary, such as public repositories, ontology-based platforms and automated meta-analysis tools. I will thus discuss some brain-atlasing resources currently under development, and their applicability in cognitive as well as clinical neuroscience.
Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
holes and slow-speed, highly variable, streams whose source regions are
under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
solar wind sources and understand what drives the complexity seen in the
heliosphere. By combining magnetic feld modelling and spectroscopic
techniques with high-resolution observations and measurements, we show
that the solar wind variability detected in situ by Solar Orbiter in March
2022 is driven by spatio-temporal changes in the magnetic connectivity to
multiple sources in the solar atmosphere. The magnetic feld footpoints
connected to the spacecraft moved from the boundaries of a coronal hole
to one active region (12961) and then across to another region (12957). This
is refected in the in situ measurements, which show the transition from fast
to highly Alfvénic then to slow solar wind that is disrupted by the arrival of
a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
Slide 1: Title Slide
Extrachromosomal Inheritance
Slide 2: Introduction to Extrachromosomal Inheritance
Definition: Extrachromosomal inheritance refers to the transmission of genetic material that is not found within the nucleus.
Key Components: Involves genes located in mitochondria, chloroplasts, and plasmids.
Slide 3: Mitochondrial Inheritance
Mitochondria: Organelles responsible for energy production.
Mitochondrial DNA (mtDNA): Circular DNA molecule found in mitochondria.
Inheritance Pattern: Maternally inherited, meaning it is passed from mothers to all their offspring.
Diseases: Examples include Leber’s hereditary optic neuropathy (LHON) and mitochondrial myopathy.
Slide 4: Chloroplast Inheritance
Chloroplasts: Organelles responsible for photosynthesis in plants.
Chloroplast DNA (cpDNA): Circular DNA molecule found in chloroplasts.
Inheritance Pattern: Often maternally inherited in most plants, but can vary in some species.
Examples: Variegation in plants, where leaf color patterns are determined by chloroplast DNA.
Slide 5: Plasmid Inheritance
Plasmids: Small, circular DNA molecules found in bacteria and some eukaryotes.
Features: Can carry antibiotic resistance genes and can be transferred between cells through processes like conjugation.
Significance: Important in biotechnology for gene cloning and genetic engineering.
Slide 6: Mechanisms of Extrachromosomal Inheritance
Non-Mendelian Patterns: Do not follow Mendel’s laws of inheritance.
Cytoplasmic Segregation: During cell division, organelles like mitochondria and chloroplasts are randomly distributed to daughter cells.
Heteroplasmy: Presence of more than one type of organellar genome within a cell, leading to variation in expression.
Slide 7: Examples of Extrachromosomal Inheritance
Four O’clock Plant (Mirabilis jalapa): Shows variegated leaves due to different cpDNA in leaf cells.
Petite Mutants in Yeast: Result from mutations in mitochondrial DNA affecting respiration.
Slide 8: Importance of Extrachromosomal Inheritance
Evolution: Provides insight into the evolution of eukaryotic cells.
Medicine: Understanding mitochondrial inheritance helps in diagnosing and treating mitochondrial diseases.
Agriculture: Chloroplast inheritance can be used in plant breeding and genetic modification.
Slide 9: Recent Research and Advances
Gene Editing: Techniques like CRISPR-Cas9 are being used to edit mitochondrial and chloroplast DNA.
Therapies: Development of mitochondrial replacement therapy (MRT) for preventing mitochondrial diseases.
Slide 10: Conclusion
Summary: Extrachromosomal inheritance involves the transmission of genetic material outside the nucleus and plays a crucial role in genetics, medicine, and biotechnology.
Future Directions: Continued research and technological advancements hold promise for new treatments and applications.
Slide 11: Questions and Discussion
Invite Audience: Open the floor for any questions or further discussion on the topic.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
This pdf is about the Schizophrenia.
For more details visit on YouTube; @SELF-EXPLANATORY;
https://www.youtube.com/channel/UCAiarMZDNhe1A3Rnpr_WkzA/videos
Thanks...!
Richard's entangled aventures in wonderlandRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
Nutraceutical market, scope and growth: Herbal drug technologyLokesh Patil
As consumer awareness of health and wellness rises, the nutraceutical market—which includes goods like functional meals, drinks, and dietary supplements that provide health advantages beyond basic nutrition—is growing significantly. As healthcare expenses rise, the population ages, and people want natural and preventative health solutions more and more, this industry is increasing quickly. Further driving market expansion are product formulation innovations and the use of cutting-edge technology for customized nutrition. With its worldwide reach, the nutraceutical industry is expected to keep growing and provide significant chances for research and investment in a number of categories, including vitamins, minerals, probiotics, and herbal supplements.
2. Rapid Neurologic Assessment
• Glasgow Coma Scale
• Response to painful stimuli—sternal rub,
trapezius squeeze
• Level of consciousness—even a subtle change
is the first indicator of a decline in neurologic
status
• Decortication—abnormal posturing seen in the
client with lesions that interrupt the corticospinal
pathways. The patient’s arms, wrists, and fingers
are flexed with internal rotation and plantar
flexion of the legs.
3. Rapid 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.
5. Brain Disorders—Migraines
Caused by a phenomenon called “cortical
spreading depression” whereby neurological
activity is depressed over a specific area of the
cortex—formerly 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 H&P, neurologic exam
and imaging.
6. Migraines
• Triggers
1. Tyramine-containing food and beverages such
as beer, wine, aged cheeses, chocolate, yeast,
MSG, nitrates, artificial sweeteners, smoked
fish
2. Medications:estrogens, nitroglycerine,
nifedipine, cimetidine
3. Other: fatigue, hormonal fluctuations, missed
meals, sleeping problems, varying altitudes
7. Commonly Used Drugs for
Migraines
• NSAIDs
• Beta blockers such as inderal
• Calcium channel blockers-verapamil
• Abortive drugs such as ASA, acetaminophen
• Ergotamine preparations
• Triptans
• Opioids
• Investigational—droperidol (Inapsine)
8. Seizures
• Abnormal, sudden, excessive,
uncontrolled electrical discharge of
neurons within the brain. May cause
change in LOC, motor or sensory ability,
and/or behavior.
• Epilepsy—chronic disorder characterized
by recurrent, unprovoked seizure activity
9. Types of Seizures
• Generalized
1. Absence—petit mal
2. Tonic-clonic—grand mal. Muscle stiffening
followed by jerking
3. Myoclonic—contractions of body muscles
4. Atonic—go “limp”, drop attacks
5. Partial—simple partial, complex partial
6. others
11. Common 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
13. Characteristics 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
14. Seizure 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 seizure—do neuro checks
15. Status 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.
16. Treatment 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
17. Meningitis
• 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 rate+25%. Most commonly
caused by Neisseria meningitidis and
Streptococcus pneumoniae.
18. Meningitis—S/S
• LOC
• Disorientation
• Photophobia
• Nystagmus
• hemiparesis
• CN dysfunction
• Personality changes
• N/V
• Fever and chills
• Red macular rash
• Nuchal rigidity, positive Kernig’s (hamstring pain w/extension) and
Brudzinski’s (flexion of the hips when the neck is flexed)
19. Review of CSF findings
• Pressure <20cm of H2O
• Clear, colorless. Cloudy indicates
infection. Pink to orange==RBCs
• Cells 0-5 lymphocytes normal.
• Glucose—50-75mg/dL normal, less than
50 indicates infection
• Proteins 15-45 normal, 45-100
paraventricular tumor, 50-200 viral, more
than 500=bacterial infection
21. Meningitis
• May display s/s of increased ICP ( see
following slide)
• Left untreated, can result in brain
herniation or damage
22. Meningitis
• Treatment according to causative pathogen as
found by LP (lumbar puncture)
• Bedrest
• IV fluids, analgesics for pain and fever
• Anticonvulsants
• Corticosteroids
• Pathogen specific abx—meningococcus
penicillin or cephalosporins, contacts rifampin or
cipro; pneumococcal—PCN, 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
24. Key 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
• Cushing’s Triad—elevated BP, decreased pulse and
decreased respirations
25. Treatment 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
26. Brain Attacks (Strokes or CVAs)
• Affects over 550, 000 Americans per year
• Two major types—ischemic and
hemorrhagic
• Caused by disruption of the normal blood
supply to the brain
• May be preventable if causes discovered
early
27. Risk Factors for Brain Attacks
• Obesity
• Heart disease
• Diabetes mellitus
• Hypercholesterolemia
• Hypercoagulable states
• Cocaine, illicit drug use
• Atrial fibrillation
28. Differential Features of the Types of
Stroke
Thrombotic—onset is gradual
• Usually related to ASHD and hypertension
• Intact LOC
• May have speech and visual changes
• Slight HA
• No seizures
• Deficits may be permanent
29. Differential of strokes
Embolic
• Abrupt
• Steady progression
• Awake
• May be associated with cardiac disease
• Maximal deficits at onset
• No seizures
• Rapid improvements
30. Differentials 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
31. Ishemic 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”
• Treatment—”clot buster” TPA,
streptokinase,others
32. Transient 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 <24h
• RINDs last >24h but less than a week
33. Hemorrhagic strokes
• If survive event, recovery from
hemorrhagic stroke better than ischemic
• Caused by vascular disruption e.g.
aneurysms, AVM
• Surgical decompression
34. Assessment of patient with brain
attack
• Neurologic exam
• Motor exam—hemiplegia vs. hemiparesis
• Sensory changes-neglect syndrome (most
notable in right cerebral hemispheric injuries)
• Amaurosis fugax—temporary loss of vision in
one eye
• Hemianopsia—blindness in one half of visual
field
• Cranial nerve function
• Cardiovascular assessment—abrupt reduction
of BP not advised
35. Assessment
• Baseline CT, MRI even better (want to
ensure that the stroke is not
hemorrhagic)
• ECG
• Echocardiogram
• Cardiac enzymes
36. Interventions
Depending of type of brain attack:
• Anticoagulants (assuming not a bleed)
• Catheter directed thrombolytic therapy—may
use if systemic tx not effective
• Endarterectomy
• Craniotomy
• Systemic thrombolytic tx—must meet strict
criteria. Must give within 3hours of onset of s/s
• Wire coils in aneurysms—seals the area
37. Key considerations
• Impaired physical mobility; self care deficit
• Disturbed sensory perception
• Unilateral neglect—in rt cerebral stroke.
May have lack of proprioception and
failure to recognize their impairment
• Impaired verbal communication—
expressive aphasia (Broca’s), receptive
aphasia (Wernicke’s)
38. Parkinson’s disease
• Genetic and environmental contributors
• Associated with four cardinal s/s: tremor,
rigidity, akinesia (slow movements), and
postural instability
• Degeneration of substantia nigra—
decreased dopamine. Acetylcholine will
predominate. Also with norepinephrine
loss thus the postural hypotension.
39. Parkinson’s 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
41. Interventions
• Eldepryl (MAO inhibitor which decreases
the breakdown of dopamine)
• Dopamine agonists—stimulate dopamine
receptors but have side effects such as
nausea, drowsiness, postural hypotension
and hallucinations. Mirapex and Requip
mimic the actions of dopamine.
42. Interventions cont.
• Levodopa/carbidopa. Used as disease
progresses. “Wearing off” phenomenon.
• Amantadine—used to treat the “wearing
off” s/s.
• Stavelo—
(carbidopa/levodopa/entacapone). Dopa-
decarboxylase inhibitor/dopamine
precursor/COMT inhibitor. Useful in end-
stage disease.
43. Drug toxicity/tolerance in PD
1. Reduce medication dosage
2. Change of medications or in the
frequency of administration
3. Drug holiday up to 10 days
44. Nursing 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 support—impaired memory
cognition
45. Surgical 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).
46. Alzheimer’s 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
47. AD
• Increased amount of beta amyloid
• Neurofibrillary tangles throughout the
neurons
• Neuritic plaques
• Granulovascular degeneration
• Reduced levels of acetylcholine
• ? Increased levels of glutamate
48. Key Features of AD
• Early-forgets names, misplaces household
items, mild memory loss, short attention span,
subtle changes in personality, wanders, impaired
judgment
• Middle—cognition vitally impaired; disoriented to
time, place and event; agitated; unable to care
for self, incontinent
• Severe-incapacitated; motor and verbal skills
lost
49. Physical Assessment of AD
• Observe for stage of progression
• Observe for changes in cognition—attention,
judgment, learning and memory,
communication/language
• 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 examination—
orientation, registration (repeat three
words), naming, reading and following
directions.
• Good one is to have them draw a clock
with an indicated time
51. Interventions 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
52. Interventions 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.
53. Interventions cont.
• Provide ID band
• Monitor to ensure safety from wandering
• Walk patient to reduce restlessness
• Involve in activities
• Restraints only as last resort
54. Multiple 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
55. MS
• Usually affects adults 20-40 years of age
• More common in women than men
• Occurs in more temperate climates
• No cure
56. MS 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
57. Diagnosis 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 protein—in
formative stages for testing at this time
58. Types
• Relapsing-remitting--charac. by remissions
and relapses
• Secondary progressive
• Primary progressive—no remissions,
gradual decline
• Progressive relapsing—steady decline
with superimposed attacks
60. Spinal 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)
61. Primary 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
62. Primary mechanisms of Injury
• Hyperextension injuries occur most often
in automobile accidents in which the
client’s vehicle is struck from behind or
during falls when the client’s 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.
63. Primary 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.
65. Extent of Injury
• Most spinal cord injuries are incomplete
lesions
• Specific syndrome result from incomplete
lesions
66. Cervical Injuries
• May produce:
1. Anterior cord syndrome
2. Posterior cord syndrome
3. Brown-Sequard syndrome
4. Central cord syndrome
• Cauda equina syndromes are associated
with injuries to the lumbar and sacral
cord
67. Cervical 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 lesion—rare. 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-Sequard—results 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 syndrome—results 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 Injuries—damage 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.
72. Vital statistics of spinal cord injuries
• Primary cause is trauma secondary to
MVA
• Unmarried male between 16-30
• Generally are Causcasian
• Most injuries are cervical
73. Assessment
• 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
74. Assessment
• 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 client’s motor and
sensory status
75. Spinal 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:
1. Flaccid paralysis
2. Loss of reflex activity below level of lesion
3. Bradycardia
4. Possible paralytic ileus
5. Hypotension.
May last days to weeks; reversal indicated by return of
reflex activity
76. Assessment
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
77. Cardiovascular
• 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 < 90 torr requires intervention to
ensure satisfactory perfusion of the spinal
ccord
78. Respiratory
• Can develop from both immobility and
from interruption of spinal innervation to
the respiratory muscles
• C3-5 innervate the diaphragm
79. Gastrointestinal and Genitourinary
assessment
• Must assess the patient’s 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.
80. Musculoskeletal 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.
81. Interventions for Patients with
Spinal Cord Injuries
• Immobilization for cervical injuries—fixed
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 injury—immobilize with
corset or brace
• Medications—supportive, may use steroids,
baclofen, other meds under investigation
82. Interventions for patients with SCIs
• Surgical decompression and
stabilization—spinal fusion, insertion of
Harrington rods, laminectomy (excision of
a posterior vertebral arch)
• Prevent complications of immobility
• Promote self-care
• Bladder retraining—spastic (UMN) or
flaccid (LMN) may be able to initiate
voiding or may need I&O catherterizations
83. Interventions cont.
• Bowel retraining—LMN may have to have
manual disimpactions, see p. 993.
• Rehab, involve community resources
• Home care management
• Psychosocial implications
84. Autonomic 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.
Can’t reach brain so reflex is activated that
increases activity of sympaathetic portion of
ANS.
85. Autonomic 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.
86. Autonomic Dysreflexia
• Precipitated by distension of the bladder or
colon; catheterization of or irrigation of the
bladder
• Is a medical emergency
87. Key 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
88. Care 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
89. Care 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
90. Myasthenia 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
91. MG
• Diagnosis based on H&P, 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)
92. MG
• 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.
93. Myasthenic Crisis
• Undermedicated with anticholinesterase
drugs.
• Increased pulse and respirations
• Rise in BP
• Anoxia
• Cyanosis
• Bowel and bladder incontinence
• Absence of cough and swallowing reflex
94. Cholinergic crisis
• Like being tx with chemical weapons
• Too much acetylcholine
• Nausea, vomiting, diarrhea
• Abdominal cramps
• Muscle twitching
• Hypotension
• Blurred vision
95. Treatment of MG
• Immunosuppression with steroids, Imuran or
Cytoxan
• Plasmapheresis
• Resp. support
• Nutritional support
• Eye protection if unable to close eyes completely
• Thymectomy
• Maintanance—cholinesterase inhibitor drugs
such as Mestinon