Patho week 10 nervous system and function

central nervous system

support and protection includes

•Skull

•Vertebral column

•Meninges

•Cerebrospinal fluid (CSF)

•Blood-brain barrier (BBB)

central nervous system

brain

•Cerebrum

•Diencephalon

•Cerebellum

•Brainstem

central nervous system

spinal cord

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What are the two main components of the peripheral nervous system?

Cranial nerves and Spinal nerves

What is the autonomic nervous system composed of?

Neurons in the CNS and PNS that mediate automatic or involuntary functions

neurons

•Cell body

•Dendrites

•Axon

glia

•Oligodendrocytes

•Astrocytes

•Microglia

•Ependymal cells

Neuronal communication

ØMembrane potentials

ØSynaptic transmission

ØNeurotransmitters

ØNeuronal circuits

neural Development

•Begins in the third week of embryonic development

•The brain continues to increase in size until puberty and remains stable until middle age

neural aging

•Normal aging

•Neurologic impairment increases with advancing age

•Excessive neuronal degeneration

•Alzheimer disease or senile dementia

neural injury

•Injury to neurons usually results in neuronal cell death and loss of function

•Some regrowth is possible in peripheral nerves if the injury is not severe

Sensory receptors

ØSpecialized terminations of the dendrites of primary sensory neurons

ØMay be a free nerve ending or may have various connective tissue elaborations that affect its responsiveness

ØDifferent receptor types respond to different kinds of stimuli

•Mechanical stretch

•Changes in temperature

Binding of chemicals

Sensory pathways

ØDorsal column-medial lemniscal tracts

•Fine touch, vibration sense, and proprioception

ØAnterolateral tracts

•Pain, itch, and temperature

Somatosensory cortex

ØOrganized in columns of gray matter that correspond to specific body locations

ØHomunculus map

Motor neurons

ØTravel from the anterior horn of the spinal cord through the ventral root and within the spinal and peripheral nerves to finally innervate target muscles

Spinal reflexes

ØAllow upper motor neurons from the brain to initiate preprogrammed movements, rather than having to excite and inhibit each an every lower motor neuron individually

Central control of motor function

ØCorticospinal tract neurons originate in the primary motor cortex, which is arranged in a similar manner to the somatosensory cortex.

ØCorticospinal neurons from the primary motor cortex, in association with neuronal output from the premotor area and the supplemental motor cortex, activate α motor neurons to execute voluntary motor commands.

Consciousness and memory

ØThoughts and memories are the outcome of activation of neurons in a neuronal circuit

ØMemories are stored by altering the synaptic efficiency of neurons in the memory trace.

ØShort-term memory: presynaptic mechanisms

ØLong-term memory: permanent changes in the postsynaptic neurons

Sleep

ØREM sleep

•Occurs at about 90 minute intervals

ØDeep sleep

ØSleep is an active process

•Sleep-inducing chemicals

Reason for sleep is unknown

Mechanisms of Brain Injury

•Brain injury mechanisms. very common

•Mechanical trauma, ischemia, cellular energy failure, reperfusion injury, excitotoxins, edema, vascular failure, and injury-induced apoptosis

•Types

•Primary

•Occurs immediately at the onset of brain injury. ex brain bleed or swelling after car crash.

•Secondary

•Development of further neurologic damage and changes subsequent to the primary injury

EX brain gets damaged from swelling that came from the car crash

ischemia

mechanism of injury

•Occurs when the delivery of oxygenated blood is less than the level needed to meet metabolic demands of the brain tissue

not enough oxygenated cells hitting tissues.

hypoxia (mechanism of injury)

•Deficiency of oxygen at the cellular level, which may occur as a result of decreased blood flow (ischemia) or decreased blood oxygenation (hypoxemia)

not enough oxygen in cells

Mechanisms of Injury - Ischemia and Hypoxia leads too

cellular energy failure (and cell death)

excitatory amino acids (can lead to free radicals)

reperfusion injury (secondary injury, injury from brain reporfusing, which is removing a clot (think picking off a scab but internal))

abnormal autoregulation (normal automatic mechanisms dont work normally)

Mechanisms of Injury - Increased Intracranial Pressure (ICP)

•Normal range: 0 to 15 mm Hg in adults (Know this!)

etiology

•Causes include stroke (CVA), trauma, tumors, other primary and secondary disorders

manifestations

•Headache, nausea, vomiting, and altered level of consciousness (LOC) (drowsiness)

Brain compression and herniation (squishing outta the one hole its got) MEDICAL EMERGENCY

•Complication of elevated ICP

•Compression of midbrain and brainstem structures is associated with rapid neurologic demise

•Herniation: protrusion of brain tissue through an opening in the supporting dura of the brain. MEDICAL EMERGENCY

management

•CT, surgery, removal of excess CSF, medication

•Goal: maintaining an ICP of less than 20 mm Hg and CPP (cerebral profusion pressure) of 50 mm Hg or greater

CPP is the pressure needed to send oxygenated blood to brain tissues

Manifestations of Brain Injury

how are we gonna "asses" it

•Level of consciousness

Use of standardized terms, confused, awake, alert, lathergic, comatose

Glasgow coma scale

•Tool used to assess LOC, here we use numbers for assessing LOC. grades awake, speech, motor response, eye movement. (lowest it can go is 3)

Cranial nerve reflexes

•Pupil reflex (shine light in em)

•Oculovestibular reflex (eyes stay on target when moving head. they dont stay straight forward) (dolls eye test)

•Corneal reflex (brush eyelashes and eyes should twitch, or take coton swab and touch eyeball if eyes are open, they should blink)

Traumatic Brain Injury (TBI)

•Epidemiology

•TBI is the leading cause of death and disability among children and young adults

•Causes include falls, sports injuries, firearms, violence, and transportation-related trauma

•Types of traumatic brain injury

•Characterized according to

•Severity (based on Glasgow coma scale, its real bad when its 8 or less)

•Location of injury (where on brain

•Mechanism of injury ( how they got it)

•

Secondary injury after head trauma refers to:

Brain injury resulting from the body's response to tissue damage

primary injury TBI

•the actual injury to brain@

Focal (focused on one area, ex brain bleed in one spot, can be minor or severe (like the brain bleed)),

polar (front and back or side to side, generally from whiplash injury (brain shift) think opposite sides),

diffuse (all over, like a shaken baby, all spots get damaged)

•Intracranial hematomas (brain bleeding) such as

Epidural hematoma (in the epidural space, from arterial bleeds, it pulses out blood, same rate as HR, damaged area expands quickly cuz its arterial. normaly from a minor injury (hitting head on a wall/other person) may loos concuousness at first then have period of lucidity (be concious) then have rapid neural deterioration in few days (its like cardiac tamponed in the skull) must DX soon! but bc those days of lucidity we may not catch it in time

.

Subdural hematoma (space btw dura and outer arachnoid, venus bleeding. oozes blood rater than shooting blood like arteries, cuz of this its more severe! symptoms are in 24 hours! poor prognosis. can have subacute ones where u get symtpoms in 2-10 days, they don't remember the injury cuz it was so long ago.

Subarachnoid hemorrhage. deepest, arterivenus malforation. where a arterie skips a capilary and just hits a vein, forms a bubble and then ruptures, leading to hemorrage, called a hemmorage cuz it doesnt gather up and clot like hematomas, it perfuses all around.

treat the three differently

scondary injury TBI

•Often the damage done by secondary mechanisms far exceeds the primary trauma

ex ischemia, increased internal cranial pressure or altered vascular pressure

TBI treatment

first thing we do is check for cardio pulmonary stabilization!!!!

then go to

Surgery, ICP management, medication, CSF drainage, seizure prophylaxis, antibiotics

based on cause!

Cerebrovascular Disease and Stroke

epidemiology

•Fifth leading cause of death and the number one leading cause of disability in the United States

•Second leading cause of death worldwide

VERY COMMON IN HOSPITALS

Ischemic stroke

•Results from sudden occlusion of a cerebral artery secondary to thrombus formation or embolization,

its like a heart attack, clot lodges somewhere in artery, disrupting blood flow, at higher risk for hypercoagulability

most often a result from a clot from a heart

AFIB puts u at high risk

starts in one min of having a clot

Hemorrhagic stroke

•Hemorrhage within the brain parenchyma

artery in the brain pops!

ppl with long-standing uncontrolled hypertension at high risk.

not as common as ischemic. thou more likley to die from it

strokes have contralateral issues, left side stroke=right side of body problems

or hemi sensory losss, half of my senses gone, right side vision gone.

can have aphasia (cant speak properly) either expressive (cant say it) or recessive (cant understand it)

strokes leads to permeanet neuro damage

so fix it fast

diagnosed with strokes severity scale and Glasgow coma scale.

as soon as we think they have a stroke, check their vitals and ENSURE CARDIO PULMONARY STABILIZATION. take em to a stat CT to look at it, we treat pregnat woman differently

two types of strokes

ischemic and hemorragic

Cerebrovascular Disease and Stroke treatment and stroke sequele

•Treatment, aimed at minimizing damag to tissue

• After airway, respiratory status, and cardiovascular function are ensured (cardiopulmonary stabiliation), stroke severity is assessed with stroke scale

•Treatment modalities differ greatly between ischemic and hemorrhagic stroke! u treat the two differently

•Treatment aimed at limiting the size of brain infarction, supporting bodily functions, and initiating aggressive rehabilitation strategies

for hemoragic we lower their bp quickly and make sure they aren't on blood thinners.

we often use surgery for both types, hemoragic we stop the bleeding, ischemic we get rid of the block.

recovery is based o how bad it was, how long it was, where it was, and how severe the squelae!, we want to start rehab ASAP bc the sooner its done the better the recovery

•Stroke sequelae

•perminet Motor and sensory deficits (minor or major, small or big) like cant move finger/arm or cant feel finger/ arm.

•Language deficits, struggle to speek or just cant do it at all.

•Cognitive deficits, langage issues, spacial relationships (how much space they take up so they run into doors). memory imparement, poor decision making.

In the acute phase of stroke, treatment is focused on what first?

Stabilization of respiratory and cardiovascular function.

Cerebral Aneurysms

most comon cause of non traumatic subarachnoic hemorages.

its the weakening of part of a artery and causes it to balloon out, then pops. most often in women! ages are often 30-60 years old)

MEDICAL EMERGENCY!!

•Etiology

•Aneurysm rupture occurs in approximately 10 in every 10,000, or approximately 30,000 individuals per year in the United States.

alcohol, smoking, high BP and cocain puts ppl at risk for it! same with family history or or being finish/japenise.

•Pathogenesis and manifestations

•Aneurysms are congenital weaknesses in the arterial walls that lead to dilation and ballooning of the wall.

graded on scale 1-5 grade 5 has a 95% chance of death!

•Sentinel leaks (warning leak, where it leaks out a little before fully poping)

severe sudden headache! worst one of their life (thunderclap headache)

symtpoms similar to migrain, photophobia (sensitivity to light) stiff neck (nukalrigidity) vomiting, neurological problems (vision issue, tingling in fingers), seizures

•Treatment

•Aneurysmal subarachnoid hemorrhage is a neurosurgical emergency, medical emergency

•Treatment options for ruptured cerebral aneurysms are determined by the aneurysm location, shape, and aneurysm neck size!

•Vasospasm is a common complication from aneurysmal subarachnoid hemorrhage, vessle clenches down which limits blood flow which can cause ischemic stroke

•Patients with aneurysmal subarachnoid hemorrhage require admission to a critical care unit

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Arteriovenous Malformations (AVM)

•Etiology

its a artery that goes straght into a vein, no capilary!

•Second most common cause of spontaneous subarachnoid hemorrhage (around 40%)

common in younger people

•More frequent in men and can rarely follow a familial pattern

Risk factors, older age, deeper AVM (its deep in brain), and having a history of it happening before to the patient)

ITS A RUPTURE

•Pathogenesis and manifestations

•Congenital malformations in which arterial blood is shunted directly into the venous system without a capillary bed, causing high venous pressure.

•The AVM enlarges and may compress adjacent structures or rupture.

often a bleed is the presenting symptom.

•Treatment

•Surgical management of rupture, radiation, or endovascular embolization to occlude the AVM may be done to prevent bleeding.

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Central Nervous System Infections - Meningitis

•Etiology

•Inflammation of the meninges (outer spot of brain, wraps around brain tissues)

•Most common sequela to microbial invasion of CNS

at risk= immunocompromised (Hiv, aids), had a organ transplants, those taking cancer treatment

can be from surgerys that F### with blood brain barier.

risk of mortality is graded by what caused it, virus vs bacterial vs fungal

•Pathogenesis and manifestations

•Most frequently, meningitis is bacterial in origin (normally strep), but it can also be viral or fungal.

we often get it from a sinus or ear infections

all have headaches, stiff necks and pyogenic (fever)

look like A##, if they are really really sick they have resptory problems, seizures, and cranial nerve deficits.

•Treatment is based off prevention

•General supportive care, empiric intravenous antibacterial drug therapy targeting the specific pathogen, corticosteroids, and management of complications

If viral, antivirals, if bacterial, general biotics, test for bacteria and target it.

Gold standerd for diagnosis is a lumbar puncture. looking for WBCs in CSF (spinal fluid), WBCs arnt normally there so if it is its bad!.

complications are optic neuritis (vision inparements), perment deffness, ongoing seizures, headache, subdural pyemia (brain infection w pus), overactive immune response if it is long term.

bacterial meningitis is a

MEDICAL EMERGENCY, can kill in 24 hours.

Central Nervous system Infections - Encephalitis

•Etiology

•Inflammation of the brain parenchyma (brain tissue)

•Pathogenesis and manifestations

•Can be caused by viruses, bacteria, fungi, and parasites, can be life threatening, more likely to be caused by a virus (ex herpes, west Nile virus and equine viruses)

unlike meningitis symptoms show up over several days,,

they have headache, fever, coma, seizures, hallucinations, psychotic behavior

•Treatment

generally, they get better in 2 weeks. treat the cause.

•Supportive and symptomatic, including fluid resuscitation, treatment of pain, and management of seizures

may need surgery to relieve skull pressure.

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Central Nervous System Infections - Brain Abscess

•Etiology

•Localized collection of pus within the brain parenchyma

normally bacterial, (often strep)

trauma and post-surgical abscesses often from staph

risk factors, lung disease, chronic sinus infection (sinusitis) chronic ear infection, bacterial endocarditis, dental abscess, injectable drugs, and immune compromise

Often in the lateral sides of brain,

•Pathogenesis and manifestations

•Pathogens reach the brain by a number of routes

•Symptoms commonly include headache, 1 to 4 weeks after the initial infection, so much later.

•Treatment depends on where its located

•Drainage or excision and long-term antibiotics are indicated.

A patient arrives on your floor after being transferred from surgical recovery and begins to have weakness in their right arm and leg. What do you think the provider will order when you call them?

CT scan

A college student living in a dormitory reports a stiff neck and headache, and is found to have a fever of 102 degrees F. This information is most consistent with:

Meningitis

Seizures and Epilepsy

chronic neuro disorders

seizures

•Transient neurologic events resulting from excessive or abnormal neuronal electrical discharges, electrical activity in brain sends impulses that shouldnt go off and body rsponds to em, like PVC

anyone can have these,

epilepsy

•Recurrent and enduring predisposition to seizures

not everyone can have these

Seizures and Epilepsy etiology and pathogenisis

etiology

•Under the right circumstances anyone can experience a seizure.

•A seizure disorder can be acquired as a consequence of cerebral injury or other pathologic process (tumor, blood clot, infection or damage to it).

pathogenisis

•Seizures result from an alteration in membrane potential that makes certain neurons abnormally hyperactive and hypersensitive to changes in their environment

we can notice a seizure when

enough cells are triggered to do something

seizures and epilepsy

clnical manifestations

diagnosis and treatments

clinical manifestations

•Seizure type such as

-Generalized onset (both sides of brain) (always lose consciousness!!)

-Focal onset (partial seizure, one side, one side of brain is having it)

-Unknown onset (we got no clue)

(what are the motor/nonmotor symptoms)

•Aura/prodrome (normally w ppl epileptic, some kind of sensation before the seizure, can be smell, sound, ect. ex smell vanilla)

DX and treatment

•Based on patient history, physical, and neurologic examination results, results of EEG studies

is this seizure one time event or does this happen often (epileptic)

protect their airway when having a seizure!

long term treatment is managed by the neurologist

cronic neuro disorders

dementia, etiology and manifestation

dimentia is considered a syndrome

•Etiology

•Characterized by progressive deterioration and continuing decline of memory and other cognitive changes!

onset can be insiduis (slow and not noticible in the begining)

initially apear disinteristed, no initiative (first sign)

•Classification: neurodegenerative (alztimers MOST COMON, parkinsons, multiple system atrophy, chronic encpholophy CTE, Prion disease (mad cow) or motor neuron (ALS)

or nonneurodegenerative (vascular dimentia, normopresure hydrocepalus, metabolic abnormalitys, depression, cancer, infections like ciphilis and HIV, vitamine B deficency!

either neurons degenerate or dont, duh

can have delirium (often in old ppl, confused, w everything, short term and get em back

dimentia is basicaly permit dilerium

•Clinical manifestations

•AD is divided into three stages

•Early (mild symptoms)

•Middle (moderate symptoms)

•Late (severe symptoms)

memory loss, short term progressing to long term

loss of executive funtion (make schedule, organize task)

anxiety (esp social)

as they progress, they have difficulty w appropriet judgment, problem solving

may need assistance w daily living in middle to late stages (bathroom)

in end stage, loose bowel control, cant eat or walk

No treatment strategy to stop progression! start off slowing then move to syptom managment

Dementia

Alzheimer disease (AD) pathogenesis

•Vascular dementia pathogenesis

•Alzheimer disease (AD) pathogenesis

•Degeneration of neurons in the temporal and frontal lobes, atrophy of the brain

•2 main Cardinal traits: β-amyloid plaques and neurofibrillary tangles (NFTs).

risk factors for AD are age, family history, personal history (head trauma) anxiety and depression.

•Vascular dementia pathogenesis

•Results from a single cerebrovascular insult (one stroke), from multiple lacunar infarcts ( a bunch of little stroke), or from microvascular pathology

when do we formally diagnose alzhimers

after death

dementia DX and treament

•Diagnosis and treatment

•Complete history and physical examination

•All manageable causes for dementia or delirium should be ruled out.

Lots of lab work.

have em draw a clock

•Medications, symptom management

DX it early is key, but there is no way to stop it, only slow it.

Before making a diagnosis of Alzheimer disease:

Other potential causes of dementia must be ruled out.

Parkinson Disease

chronic neuro disorders

etio patho

•Etiology

•Progressive neurodegenerative disorder characterized by bradykinesia, rigidity, tremor, and postural instability (balance issues)

•May be idiopathic (slow) or acquired (fast) (infection, intoxication including alc/drugs, trauma)

more common in older ppl

•Pathogenesis

•Results from degeneration and loss of the pigmented dopaminergic neurons found in the substantia nigra pars compact and, to a lesser extent, neurons elsewhere in the brain

Dopamine receptors!

•Intraneuronal Lewy bodies inclusions com

most of the dopamine receptor neurons are dead before the patient knows theres a problem

Parkinson Disease

clinical manifestations

treatment

•Clinical manifestations

•Difficulty initiating and controlling movements results in akinesia, tremor (a rest tremor, when doing something it stops but at rest it gets funky, can become very severe looking, almost seizure looking, is often what sends patient to doc to get check up. often starts on one side and progresses to other), and rigidity. (often ignored or confused w other things). slow walking, shuffling feet, loose ability to make facial expressions, less blinking.

all of these get worse over time

•Treatment

no cure. just slow progression and manage symptoms

•Medication (forms of dopamine), antidepressant therapy, surgery for the tremors

The classic manifestations of Parkinson disease include:

Rest tremor and skeletal muscle rigidity

Clinical Manifestations of Parkinson Disease

TRAP

Tremor

Rrigidity

Akinesia (loss of voluntary muscle use)

Posture and balance

Cerebral Palsy

cronic neuro disorders

etiology and patho

•Etiology and pathogenesis

•Group of crippling syndromes that appear during childhood and involve permanent, nonprogressive damage to motor control areas of the brain

•Etiologic factors: prenatal infections or diseases of the mother; mechanical trauma to the head before, during, or after birth; or exposure to nerve-damaging poisons or a period of reduced oxygen supply to the brain

F#cks with voluntary and involuntary movments•

can be mild or severe (which is at risk for lifelong complications)

often have chronic pain

Cerebral Palsy

clinical manifestations

treatment

•Clinical manifestations

•May be classified by neurologic signs and symptoms involving spasticity, ataxia, dyskinesia, or a mix of two or more of these three symptoms

can have hypertonia (big muscles)

seizures, mental difficultys, memory issues, intelectual problems

chronic pain

•Treatment

no cure, increase functionality as best as possible

•Muscle relaxants, anticonvulsant drugs, orthopedic surgery, casts, braces for walking, traction for walking

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Hydrocephalus

chronic neuro disorders

water (CSF) in the brain

•Etiology

•Characterized by abnormal accumulation of cerebrospinal fluid (CSF) in the cerebral ventricular system

•May be acquired (infection, cancer) or congenital

can be obstructive or reabsorption

•Pathogenesis and clinical manifestations

•Types of hydrocephalus:

normal-pressure hydrocephalus (0-15,

obstructive hydrocephalus, has increased Cranial pressure cuz we cant get CSF out

communicating/non obstructive hydrocephalus (an reabsorption one

seen in 5 years of age

•Treatment is the same, based on age

•Surgical correction using a shunt (drain tube)

•infants have room to expand, so head expands out

adults dont cuz bones fused. have headaches, confused, nausia, poor vision, all we can do is surgery!!!

Multiple Sclerosis (MS)

chronic neuro disorders

etiology and patho

•Etiology

• Chronic demyelinating disease of the central nervous system (CNS) that primarily affects young adults (20-40).

effects the spinal cord!

3x more common in women, and more common in white ppl

•Greater risk for persons living in higher latitudes.

breaks down and myelin sheaths by sclerosing (hardening) them till they break.

we dont know the cause, we think viral/ autoimmune/ genetic predisposition in nature

•Pathogenesis

•Demyelination can occur throughout the CNS but most frequently affects the optic and oculomotor nerves and spinal nerve tracts.

•

Multiple Sclerosis (MS)

clinical manifestations and

treament

•Clinical manifestations and treatment

•Double vision, weakness, poor coordination, sensory deficits, loss of bowel and bladder control, memory impairment, anything that ramps up an immune response (heat, infection, ect)

4 types

relapsing/remiting

primary progressive,

2ndary progressive,

prolapse/ progressing

•Management is symptomatic. no cure

•Short-term steroid therapy may be helpful during acute exacerbations, and immune-modifying drugs may slow the progression of symptoms.,

anti spasmotics may help with the symptoms, same with anti colonergics, anti depresents, and anti microbial too.

diagnosed w 2 or more of these exacerbations, coupled with imaging results showing its pathology in the nervous system

Spina Bifida

•Etiology and pathogenesis

•Developmental anomaly (happens in utero) characterized by defective closure of the bony encasement of the spinal cord (neural tube) through which the spinal cord and meninges may or may not protrude

happens in week 4 of gestation

folic acid deficiency in mom is most common cause

meds mom takes can cause it too

•Clinical manifestations

•Types: spina bifida occulta (hidden, can't see the closed off part), but have symptoms like cant use lower extremity), spina bifida cystica (have a cyst like structure on lower portion of back, U can see it)

myloningiseal has to do w cystica, they contain spinal fuild and some of the spinal cord! nearly always on the lower lower back! like sacral.

meningeocele has no spinal code

for Cystica almost always super weak or paralyzed, may never recover, symptoms get worse as they grow

•Treatment based of how bad the defect is.

DX before birth w ultrasound except for occultsa, its hidden so u spot them by seeing dimple in back, hair in back of body on bump, lipoma in back, lack of lower leg movement, difficulty walking, malformed feet, and bowel disfunction

may have surgery after first few days of birth

•Early and aggressive operative approach before significant clinical deterioration begins

•Preventive measures: folic acid supplementation before conception and during pregnancy

________ is a form of spina bifida in which a saclike cyst filled with CSF protrudes through the spinal defect but does not involve the spinal cord.

meningeocele

Amyotrophic Lateral Sclerosis (ALS)

•Etiology and pathogenesis

•Progressive disease affecting both the upper and the lower motor neurons

age 40

more common in men

•Clinical manifestations and treatment

•Diagnosis of exclusion

•Manifestations: (starts with) weakness, atrophy (of limbs), cramps, stiffness, and irregular twitching of muscle fibers, sometimes dementia

leads to progressive paralysis and death in 3-5 years

•Management: medication, prevention of complications, supportive care

•Mean survival time: approximately 3 years from time of diagnosis

DX of exclusion just like alzheimers, we rule everything else out first. using MRIs and other imaging

No cure, just trying to help make them more comfortable, nto even slowing it down!

Spinal Cord Injury

•Etiology and Pathogenesis

•Usually traumatic

more common in young ppl and in men

•Cord may be compressed (can be trauma, tumor, fracture), transected, or contused

hyperextension injurys are most common!

•Further injury may result from hemorrhage, swelling, and ischemia after injury

may be primary or secondary (from swelling ect)

clasified off of lvl of injury, degree of injury, and how we did it

•Clinical manifestations

•Spinal shock (generally all loss of function below level of injury, complete flaccidity of em all, it is going away when reflex's are coming back)

•Neurogenic shock (cervical or uper thoracic spinal injury, loss of some centeral nervus system function below the spot!)

•Autonomic dysreflexia' ( can happen any time after spinal injury at T6 or higher! even 5 years ago, has hypertentsion, headacher, bradychardia, upper body flushes turning read and has vasoconstriction in lower body. comes from visceral pain receptor below spinal injury being triggered, these patients are parlized btw)

•Treatment depends on where it is

•Surgery, medication (high dosed sterioids to decrease inflamation), oxygen, prevention of complications, supportive care, stabilization

if go into shock go to ICU (duh)

Guillain-Barre Syndrome

•Etiology and pathogenesis

inflamatory demylenating disease of the peripheral nervus system, esp the lower spots!

•Heterogenous syndrome with multiple variants

•Postinfectious immunologic mechanism such as cross-reactive antibodies to peripheral nerves is suspected

can be from virus, ex epstine bar, can be from autoimmune response to a vaccine

•Clinical manifestations and treatment

•Symptoms include muscle weakness that begins in the lower extremities and spreads to the proximal spinal neurons. ( so it goes up)

•Treatment: supportive,

•Spontaneous recovery, it works on its own generally. heals opposit way of progressing, gets better from top and moves down.

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Facial Nerve Palsy or Bell Palsy

•Etiology and pathogenesis

an acute problem

idiopathic facial nerve palsy is bell palsy

•Paralysis of the muscles on one side of the face

•Often a self-limiting condition with unknown cause. like from a infection.

15-45 years old

diabetics, hypothyroidism and pregnant patients are at risk.

•Clinical manifestations and treatment

•Unilateral facial weakness and facial paralysis in 48 hours with facial droop and diminished eye blink, hyperacusis, decreased lacrimation

ROLE OUT STROKE FIRST!!!

•May last only a few days or weeks.

•Treatment: supportive, ex keep eyes damp cuz it can mess w it, give em steroids for inflammation.

•Spontaneous recovery, heals self in few weeks

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