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Meningitis
Inflammation of the meninges and subarachnoid space; CSF may also become infected
Caused by: bacteria(more severe)- group B strep, Neisseria, Streptococcus pneumoniae, Haemophilus influenzae, and Viruses: enterovirus, West Nile virus, HIV, herpes
infection or irritant tirggers inflammation leading to swelling or meninges and increased intracranial pressure(ICP)
Meningitis
risk factors
younger than 25, living in community setting(dorms), pregnancy(listeria), working with animals, immunodeficiciency
Meningitis can be
viral, bacterial
viral- self limiting
bacteria- life-threatening(rapid, severe)
Meningitis
manifestations
complications
mimics flu symptoms: fever, chills, LOC, N/V, photophobia(light sensitivity), severe headache, nuchal rigidity(stiff neck), bulging fontanelles(infants), poor feeding or irritability in children, tachypnea, tachycardia, rash
permanent neurologic damage(hearing loss, blindness, speech difficulties, learning disabilities, behavior problems), seizures, paralysis adrenal gland failure(caused by the Neisseria bacteria), cerebral edema, shock, death
Encephalitis
MORE SEVERE THAN MENINGITIS
Inflammation of the brain and spinal cord, usually from an infection
Caused by bacteria: lyme disease, TB, syphilis and viral(coxsackievirus, echovirus, poliovirus, adenovirus, herpes, cytomegalovirus, eastern equine, west nile, st loius, measles and mumps
infection triggers inflammatory response—> vasodilation, increased capillary permeability, leukocyte infiltration(increased WBC)
Encephalitis may be
primary(direct viral infection of the brain or spinal cord)
secondary(travels from elsewhere in the body)
Most cases are mild and self-limiting, but can be severe and life-threatening
Vulnerable groups: immunocompromised, young children, O.A., high-incidence area
Encephalitis
manifestations
complications
Most cases are mild and go undetected
Symptoms are similar to meningitis but with a more gradual onset: flu symptoms, headache, bulging fontanels, neck rigidity, photophobia, diplopia, seizures, ataxia, weakness, LOC, paralysis, tremors, rash
confusion, hallucinations, personality changes, paresthesia, abnormal deep tendon reflexes
nerve cell degeneration, cerebral edema, cerebral hemorrhage, and brain damage
Zika Virus Disease
Caused by a flavivirus
outbreaks in Africa, the Americas, Asia, and the Pacific
Brazil: 2015 - large outbreak —> neurologic complications
Transmission: mosquito(primary), foreign travel, sexual transmission(virus lives longest in semen)
other sources: mother to fetus, blood transfusion
Zika can cause Guillain-Barre syndrome(persons own immune system is attacking their own nerves—>paralysis and weakness)
BABIES BORN WITH SMALL HEADS
higher risk of miscarriage and contracture
Increased Cranial Pressure(ICP)
Results from increased pressure in the cranial cavity(3 components: brain tissue, CSF, blood)
Caused by traumatic brain injury, tumor, hydrocephalus, cerebral edema, and hemorrhage
Monro-Kellie hypothesis: increase in volume of one component must be compensated for by a decrease in volume of another(1 volume increases, another decreases); usually shifts are in CSF and blood because brain tissue does not move easily
2 other compensatory mechanisms for ICP:
Autoregulation: the blood vessels will dilate to increase blood flow and constrict if ICP increases
Cushing’s reflex: the hypothalamus increases sympathetic stimulation when the mean arterial pressure drops below the ICP —→
CUSHING’S TRIAD(IMPORTANT): increased blood pressure, bradycardia, and Cheyne-Stokes respirations(deep, fast breathing—→periods of apnea)
Herniation
Feared complication of increased ICP
Refers to displacement of brain tissue(if CSF and blood flow can’t accomodate)
push downward on brainstem

Manifestations of Increased ICP
Common: decreasing LOC, vomiting(projectile); from pressure on medulla, Cushing’s triad, fixed and dilated pupils, posturing(decorticate: towards the core, decerebrate: away from the core)
Infants: separated sutures and bulging fontanelle
Older children and adults: behavior changes, severe headache, lethargy, neurologic deficits, and seizures
Hematoma
Collection of blood in the tissue that develops from ruptured blood vessels
Hematomas can develop immediately or slowly because of a traumatic brain injury(TBI) or surgery(some kind of trauma)
Epidural Hematoma
Bleeding between the dura and skull(EPI-DUR), usually caused by an arterial tear
An arterial tear is larger and more severe than a venous rupture
Manifestations: neurologic dysfunction that develops within a few hours of injury
symptom pattern: brief LOC—→short period of alertness—>LOC again
Subdural Hematoma
Between the dura and the arachnoid, usually caused by a small venous tear
develops slowly; manifestations are present within 24 hours of an injury
progresses rapidly and has a high mortality
ICP increases over a period of about a week after the injury
Chronic subdural hematomas: elderly adults associated with brain atrophy: manifestations develop slowly after injury because of slow leak
Intracerebral Hematomas
Bleeding within the brain tissue
caused by
contusion or shearing injury
HTN
CVA(strokes)
aneurysms, or vascular abnormalities
Subarachnoid Hemorrhage
Bleeding in the space between the arachnoid and pia
Primary clinical presentation:
⚬ Severe headache with a sudden onset that is worse near the back of the head
Hematoma complications
Bleeding—→localized pressure on tissue—>increased ICP
blood may coagulate and form a solid mass
Fluid from the hemolysis exerts osmotic pressure, drawing more fluid into the capsule —→ edema increases the mass size, applying more pressure and increasing ICP
bleeding can trigger vasospasm and ischemia
Can result in herniation of brain tissue
Spinal Cord Injury
results from
caused by
Result from direct injury to the spinal cord or indirectly from damage to surrounding bones, tissues, or blood vessels
direct damage if cord is pulled, pressed sideways, or compressed
Caused by motor vehicle accidents, falls, violence, sports injuries, and weakening vertebral structures(RA and osteoarthritis)
What can occur inside or outside the spinal cord after a spinal injury?
Hemorrhage(bleeding), fluid accumulation, and edema(occurs inside or outside spinal cord, but within spinal canal)
Spinal Shock:
most common in which demographic
Temporary suppression of neurologic function because of spinal cord compression; neurologic function gradually returns
caucasians and males; average age has increased from 29 to 43
Spinal Cord Injury: Complications
loss of neurologic function
varying degrees of paralysis
Cauda equina syndrome(medical emergency): injury to the nerve roots in the area of the cauda equina —→ can cause bladder and bowel dysfunction, pain/altered sensation in legs, loss of sexual sensation, saddle numbness(pelvis)
Another spinal cord injury complication:
autonomic hyperreflexia
Massive sympathetic response that can cause headaches, hypertension(HYPERTENSIVE CRISIS), seizures, stroke, and death
associated with injuries above T6
noxious stimuli triggers cascade(look at diagram)

Spinal Cord Injury: Manifestations
Manifestations are usually below the level of injury
Cervical injuries: C4 and up
upper and lower extremities; breathing difficulties, loss of bowel and bladder control; paresthesia; spasticity; pain; weakness; paralysis; BP instable; temperature fluctuations; diaphoresis
Thoracic: trunk and lower extremities
similar manifestations as cervical, but no breathing difficulties here
Lumbar sacral injuries
lower extremeties impacted; bowel and bladder dysfunction, may need to walk in a wheelchair or brace

Another Spinal Cord injury complication: Neurogenic shock: (compare to autonomic hyperreflexia)
An abnormal vasomotor response secondary to disruption of sympathetic impulses
⚬ Hemodynamic impact (DECREASED HR & BP)
Respiratory failure,
Effects of immobility(constipation, pulmonary infection, UTI, thrombus, impaired skin integrity, contractures)
bowel and bladder dysfunction
sexual dysfunction
chronic pain
death
Autonomic hyperreflexia can happen at any time after injury; neurogenic shock happens more acutely
Side by side diagram

Vascular Neurological Disorders: Transient Ischemic Attack (TIA)
what is it
what is it caused by
what does it mimic
TIAs are a warning sign for what
A TEMPORARY episode of cerebral ischemia that results in symptoms of neurologic deficits (“mini stroke”)
Causes: cerebral artery occlusion(e.g., thrombus, embolus, or plaque); cerebral artery narrowing(e.g., atherosclerosis or spasms), or cerebral artery injury (e.g., inflammation or hypertension)
neurologic deficits mimic a CVA(stroke) except these deficits resolve within 24 hours(usually 1-2 hours)
may occur single or in a series
TIA can be a warning sign for a stroke, but not all CVAs are preceded by a TIA
1/3 who have a TIA eventually have a stroke
half of these CVAs occur within 1 year of TIA
TIA Risk Factors
Smoking, DM, bad diet, hypercholesterolemia, older age, oral contraceptive, excessive alcohol, and illicit drug use
TIA Manifestations
begin suddenly and last shortly
same as for a stroke(reflect the location of ischemia)
Permanent brain damage, injury from falls, and CVA
BEFAST
B: loss of Balance, headache, dizziness
E: blurred vision
F: facial drooping
A: arm or leg weakness
S: speech difficulty
T: time to call for an ambulance immediately
Muscle weakness or paralysis(face, arm, or leg unilateral), ataxia, changes in sensation: agnosia-inability to recognize or identify sensory stimuli, aphasia(speaking), dysphagia(swallowing), dysgraphia(writing), diplopia, nystagmus, vision loss, difficulty reading, change in LOC, confusion, personality/mood changes, vertigo, incontinence
Vascular Neurological Disorders: Cerebrovascular Accident (CVA)
what is it
what does it interrupt
caused by
stroke, or brain attack
interruption of cerebral blood supply
ischemic damage is permanent
Causes: ⚬ Total vessel occlusion (e.g., thrombus, embolus, or plaque) or cerebral vessel rupture (e.g., cerebral aneurysm, arteriovenous malformation, or hypertension)
Two major types of CVA
ischemic strokes: most common
hemorrhagic strokes: most fatal
CVA
complications
most common in
risk factors(similar to TIA)
neurologic deficits and death
Most common in African Americans and people living in the Southeast region
Additional risk factors: ⚬ Physical inactivity, stress, obesity, hypertension, smoking, dyslipidemia, diabetes mellitus, atherosclerosis, oral contraceptive usage, excessive alcohol consumption, illicit drug use, and advancing age
CVA Manifestations
Similar to those of TIA, except they do not resolve
may improve with time and therapy, but they can remain —→complications
Additional manifestations: headaches with hemorrhagic strokes because of increased ICP
Vascular Neurological Disorders: Cerebral Aneurysm
what is it it
causes(similar to CVA and TIA)
A localized outpouching of a cerebral artery due to weakening of the artery wall
can put pressure on surrounding tissue; as well as leak or rupture; causing or CVA or death
Common causes:⚬ Congenital defects, hypertension, diabetes mellitus, dyslipidemia, connective tissue diseases (e.g., Marfan syndrome), traumatic brain injuries, arteriovenous malformations, cigarette smoking, illicit drug use, and brain tumor
Cerebral Aneurysm
most frequent type
where does it occur
when does it cause symptoms
Manifestations:
Most are berry or saccular
Most frequently occur in multiples on the circle of Willis
Usually asymptomatic until they grow large or rupture
vision issues(diplopia and vision loss), headache, eye pain, and neck pain
Sudden, severe headache is an indication that the aneurysm has ruptured; may resemble symptoms of increased ICP and CVA
Headache disorders
Another name for headache; where does pain occur
characterized by
where can the headaches occur
what kind of pain
onset of pain
cephalalgia: refers to pain in any region of the head
recurrent headaches
one or both sides, one area, radiate across the head, or have a vise-like quality
sharp, throbbing, or dull
develops gradually or suddenly, last hours to days
Primary headache disorders
caused by
examples
No apparent underlying cause
migraines, tension type headaches(TTH), trigeminal autonomic cephalagias(TACs)
genetic and environmental factors(chemical activity, nerves, blood vessels, muscles of the brain, head, and neck)
Secondary headache disorders:
causes
Red flag symptoms
Less common
underlying causes: tumors, infections, hemorrhage, aneurysm, cerebral arteriovenous malformation, acute sinusitis, otitis media, concussion, dehydration, dental problems/infections, glaucoma, hangovers, carbon monoxide poisoning, monosodium glutamate ingestion, altered CSF pressure or volume, and skull deformities.
if you fix the cause, then the headache goes away
Red flag symptoms: thunderclap headache; new-onset headaches; persistent morning headache with nausea; headaches that get worse over time; headaches associated with postural changes; and aura symptoms that last longer than an hour(indication that headache is coming on-could be visual like seeing dots, neck pain, impaired balance)
Seizure
What is it
primary causes
secondary causes
transient physical or behavior alteration that results from an abnormal electrical activity in the brain
• Primary Causes: ⚬ Altered membrane ion channels ⚬ Altered extracellular electrolytes ⚬ Imbalanced excitatory and inhibitory neurotransmitters
Secondary Causes :⚬ Trauma, hypoglycemia, electrolyte disorders, acidosis, infection, fever, chemical ingestion(e.g., medications, illicit drugs, and alcohol),cerebral ischemia or hypoxia
Epilepsy
what is it
characterized by
complications
seizure disorder resulting from spontaneous firing of abnormal neurons;
characterized by recurrent seizures; there is no underlying or correctable cause
Complications: Brain damage • Traumatic brain injury • Aspiration• Mood disorders • STATUS EPILEPTICUS: seizure activity lasting longer than 5 minutes or subsequent seizure(s) that occur before the individual has fully regained consciousness within this timeframe
The two different kinds of seizures
postictal period
Focal and Generalized
not all can be easily defined as either focal or generalized
some begin as focal and spread to the entire brain
some people may have both types of seizures with no clear pattern
Postictal period: just after the seizure, the individual will be confused, fatigued, and fall into a deep sleep
Focal Seizure
also called partial seizure
occurs in just one part of the brain
manifestations vary depend on part of brain being affected
Frontal lobe: movement, emotions, memory, language, social/sexual behavior, and personality
Temporal lobe: hearing, speech, memory, emotions
Parietal lobe: bodily sensations
Occipital lobe: processing vision
Brain stem: breathing, hr, temperature
Cerebellum: balance and coordination
Generalized Seizure
Abnormal neuronal activity on both sides of the brain • May cause loss of consciousness, falls, or massive muscle spasms
many different types…
Absence seizure(previuosly called petit mal seizure)
individual may appear to be staring into space and/or have jerking or twitching muscles
often missed
Tonic seizure
causes stiffening of muscles of the body, generally those in the back and extremities
Clonic seizure
causes repeated jerking movements of muscles on both sides of the body
Tonic–clonic seizure (previously called grand mal seizure):
causes stiffening of the body and repeated jerks of the arms and/or legs as well as loss of consciousness
Myoclonic seizure
causes jerks or twitches of the upper body, arms, or legs
like when you fall asleep and suddenly jerk awake
Atonic seizure:
causes a loss of muscle tone; will fall down or may drop his or her head involuntarily•
Chronic Degenerative Disorders: mulitple sclerosis
what is it
how does damage occur
Debilitating autoimmune condition: progressive and irreversible demyelination of brain, spinal cord, and cranial nerves
Damage occurs in diffuse patches throughout the nervous system and slows or stops nerve impulses
Progression of the damage varies

Who is MS most common in?
what age do symptoms onset
what are complications
characterized by
may progress without…
Most common in women, caucasians, and those living in temperate climates
symptoms onset between age 20 and 40
complications: epilepsy, paralysis(legs), and depression
varying depending on degree of damage to nerves
characterized by remissions and exacerbations; which may last for days to months
may progress without remission
Multiple Sclerosis Manifestations
really think about those slowing nerve impulses
MS more conitive manifestations
Sensory: Vision issues (e.g.,diplopia and vision loss);Slurred speech; Paresthesia; Hearing loss
• Fatigue; Dizziness
• Decreased attention span, poor judgment, and memory loss
• Difficulty reasoning and solving problems
• Dysphagia
• Problems moving arms or legs
• Weakness and/or tremor in one or more arms or legs
• Ataxia; Unsteady gait; Muscle spasms
• Constipation and stool leakage
• Urinary frequency, urgency, hesitancy, or incontinence
• Sexual dysfunction
Amyotrophic Lateral Sclerosis
aka
damage to what
What is not affected
nerves lose their ability to…
increases risk for what?
Lou Gehrigs disease
damage to upper motor neurons of cerebral cortex and lower motor neurons of brain stem
Sensory neurons, cognitive function,and cranial nerves III, IV, and VI arenot affected
Nerves lose their ability to trigger rmuscle movement, resulting in muscle weakness, disability, paralysis, and eventually death (usually within 3years of onset of symptoms)
• May also increase the risk for dementia
Amyotrophic Lateral Sclerosis
causes
Upper motor neurons
Lower motor neurons
manifestations
no definitive cause; genes and environment
ALS people lack the enzyme that protects cells from free radical damage
excess glutamate(toxic to nerves)
A.I. response
Upper motor neurons—→spastic paralysis and hyperreflexia
Lower motor neurons—→ flaccid paralysis
Manifestations: foot drop, lower extremity/upper extremity/hand weakness and clumsiness, walking difficulty, twitching in upper extremities and tongue, choking, unbalanced
ALS and MS similar manifestations
walking difficulty, weakness in legs/arms, slurred speech, dysphagia, muscle cramps
Chronic Degenerative Disorders: Parkinson’s disease
what is it
what does it result in; when 80% of…
when do tremors decrease
cause
more common in who?
Progressive condition involving the destruction of the substantia nigra in the brain
Results in a lack of dopamine
When 80% of the dopamine-producing cells are destroyed, movement issues typically include tremors of the hands and head develop
tremors may decrease when the body part is moved intentionally
cause: unknown
more common in men and those living in rural area
Parkinson’s Disease Manifestations
REMEMBER THESE: slowing or stopping automatic movements(blinking), masklike appearance, difficulty initiating or continuing movement(walking or getting out of a chair)movement, loss of fine hand movements(writing, eating), shuffling/unsteady gait, slowed movements
constipation, urinary hesitancy or urgency, dysphagia, drooling, anosmia(loss of sense of smell), myalgia

Parkinson’s Disease Manifestations: Tremors
where do they occur/when
eventually tremors happen where in the body
when are they worse
example
occur in limbs at rest or while held out, go away during purposeful movement
eventually seen in the head, lips, tongue, feet
may be worse when tired, excited, stress
example: finger-thumb rubbing(pill-rolling - tremor)
Huntingtons Disease
Autosomal dominant; chromosome 4 (increased chance of getting the disease the further it gets passed down genetically)
genetically programmed degeneration of neurons
atrophy of the brain(basal ganglia and frontal cortex)
Most cases appear at age 30-40
10-30 years to live
Huntingtons Manifestations
initially insidious
family members may report unusual behaviors: mood swings, irritable, depressed, angry, antisocial, hallucinations, paranoia, psychosis * commonly mistaken for psychiatric disorder
Early signs: trouble driving, learning new things, answering questions, remembering facts
Myasthenia Gravis
pathway
muscles involved
A.I. condition
acetylcholine receptors are destroyed by IgG autoantibodies—→disrupts normal connection between the nerve and muscle at the neuromuscular junction
Weakness of voluntary muscles due to decreased nerve stimulation
muscle weakness increases during activity and improves after rest
muscles of Eye, eyelid movement, facial expression, talking, chewing, and swallowing
muscles that control breathing, neck, limb movement
MA triggered by
myasthenic crisis
factors that worsen and cause myasthenic crisis
unclear
thymus abnormalities, hyperthyroidism, A.I disorders
Myasthenic crisis: life-threatening: muscles too weak to breathe
fatigue, illness, stress, heat, alcohol, meds(beta blockers, calcium channel blockers, quinine, antibiotics)
MG manifestations
difficulty climbing stairs, lifting objects, or rising from seated position
dysarthia(motor speech)
eye, vision issues
drooping head
facial paralysis
fatigue, hoarseness, changing voice
breathing difficulty
dysphagia
Dementia
what is it
what skills does it impair
issues with what
group of conditions in which cortical function is decreased
impairing cognitive skills and motor coordination
Issues with memory; short memory losses and confusion about historical events
Behavior and personality changes interfere with relationships, work, and ADLs
Types of dementia
dementia is an umbrella term
⚬ Alzheimer’s disease
⚬ Vascular dementia
⚬ Dementia with Lewy bodies
⚬ Frontotemporal dementia
⚬ Creutzfeldt-Jakob disease
⚬ AIDS dementia complex
Alzheimers
most common form of…
what happens to brain tissue
associated with what three pathologic characteristics
Most common form of dementia
brain tissue degenerates and atrophies causing a steady decline in memory and mental abilities
amyloid plaques mix with proteins, neuron remnants, and nerve cell pieces
Neurofibrillary tangles: abnormal collections of a protein called tau that clumps together
Connections between neurons responsible for memory and learning are lost: neurons cant survive if connection to other neurons are lost
Alzheimers
what kind of aging
higher rates in who
additional risk factors
complications
abnormal aging, risk increases with age
rates higher in women, and those with less education
Additional risk factors: fx, HTN, hypercholesterolemia, DM, TBI
prevalence + mortality rates on the rise
complications: infection(pneumonia, UTI), fall injuries, malnutrition, dehydrations, ulcers
Alzheimer’s manifestations
insidious onset
10-20 years
Memory loss, problems with abstract thinking, difficulty finding the right word to express thoughts or even follow conversations, difficulty reading and writing, disorientation (even in familiar surroundings), loss of judgment, difficulty performing familiar tasks, personality changes, hallucinations, and incontinence of bowel or bladder
Brain tumors
may be malignant or benign
can be life threatening due to increased ICP and difficulty assessing
may be primary, but most are secondary(breast, colon, kidney, lung, melanoma, sarcoma)
brain tumor cont
Primary tumors are thought to arise from genetic mutations
• Risk factors for primary tumors: ⚬ Advancing age; exposure to radiation and occupational chemicals
• Prevalence and mortality rates are highest among Caucasians and males
• Complications: ⚬ Neurologic deficits ⚬ Seizures , Personality changes ⚬ Death
Brain Tumor Manifestations
Vary depending on size and location
new onset or change in headaches
headaches increasing in frequency and severity
unexplained N/V
vision problems
gradual loss of sensation and movement
balance difficulties, speech difficulties, hearing problems, hormone(endocrine) disorders