Neuro Flashcards
Cranial Nerves
On Old Olympus Towering Tops A Fin and German Viewed Some Hops
1 Olfactory -Smell
2 Optic -Vision
3 Oculomotor -EOM, eyelid opening, pupillary constriction
4 Trochlear -Downward and inward eye movement
5 Trigeminal - Mastication, sensation face, mouth, nose
6 Abducens -Lateral eye movement
7 Facial -facial movement, eye/mouth closing, taste, saliva/tear
8 Acoustic -Hearing and equilibrium
9 Glossopharyngeal -phonation, posterior taste, gag, carotid, reflex, swallow
10 Vagus-Talking, swallow, sensation carotid body, carotid reflex
11 Spinal Accessory- (shrug) trapezious/sternocledomastoid
12 Hypoglossal- moves the tongue
Sensory/ Motor / Both
Some
Say
Marry
Money
But
My
Brother
Says
Big
Bras
Matter
Most
WHat is the timeframe for and symptoms of TIA?
Periods of cerebral insufficiency with < 24 hours with NO residual effects
TIA indicative of pending stroke (1/3 infarct w/in 5 yrs)
Infarctions more common (80%) than hemmorrhage (20%)
Sx:
- amaurosis fugax (ipsilateral monocular blindness)
- Transient aphasia
- Parathesias of contralateral limbs or face
- Nystagmus, vertigo, dysphagia, sensory deficits
*Same side eye changes, opposite motor changes
TIA Classifications
Vertebrobasilar: inadequate blood flow vertebral arteries
*neuro like symptoms (vertigo, ataxia, dizziness, VF deficits, weakness, confusion)
Carotid:carotid stenosis (more traditional stroke life symptoms including aphasia, dysarthria, altered LOC, weakness, numbness
TIA Dx
Dx:
- CT best for distinguishing between ischemia, hemorrhage, tumor
- MRI superior to CT for ischemic infarct
- Echo
- Carotid Doppler/US
- Cerebral Angio
TIA Management
ASA
Plavix superior choice
Ticlid-needs lab monitoring for agranulocytosis & thrombocytopenia
Assess for HTN *#1 cause heart failure
Carotid endart indicated for >70-80% stenosis in symptomatic pts, decreases risk for stroke/death in recent TIA
CVA Definition
Rapid onset of neuro defecits > 24 hrs duration
- 4th leading cause of death
- Can be subtle, progressive or sudden onset
CVA causes
- Atherosclerosis
- Chronic HTN
- Trauma
- Aneurysm
- AV Malformation
- Tumor
Hemorrhagic CVA
Presents with acute onset of focal neuro defecits
Hemorrhagic CVA signs and symptoms
Sudden increased ICP including altered mentation, HA, vomiting when extensive
*
Hemorrhagic CVA Diagnostics
- Head CT
- Cerebral angio
- Lumbar puncture if Grade I or II aneurysm for blood in CSF (do CT first)
CVA Management
- Surgical evaluation
- Lower systemic BP while avoiding hypotension
- Prevent sudden increased ICP:
- Elevate HOB, Sedation, Oxygen, Analgesic, Laxative
- MAP 110-130 to treat cerebral vasospasm
- Intravascular volume expansion and HTN tx to increase cerebral perfusion (CPP=MAP-ICP)
- Nimodipine (Ca Channel agonist) to counter vasospasm
*Maintain CPP and limit increases in ICP to <20
ICP H’s
Hypertension
Hypoxia
Hypercapnia
- Tx by hyperventilation, keep CO2<35, O2 high and maintain higher MAP’s 110-130 (increases vital organ perfusion and prevents cerebral vasospasm)
Simple Partial Seizures
Simple Partial (focal, local)- common with cerebral lesions
- No loss of consciousness
- Rarely lasts >1 min
- Motor sx start with single muscle group and spread to entire side of body
- Paresthesias, flashing lights, vocalizations, hallucinations
Complex Partial Seizures
Any partial seizure followed by impaired LOC
- May have aura, staring, automatisms such as lip smacking or pulling at clothing
Generalized Seizures
Absence (petit mal)
- Sudden arrest of motor activity with blank stare
- Common in children/adolescents
- Begin and end suddenly
Tonic-Clonic (Grand mal)
- May have aura
- Begins with repetitive involuntary contraction of muscle (tonic clonic)
- Ususally lasts 2-5 min
- Incontinence possible
- Followed by post-ictal period
Status Epilepticus
Series of Grand-Mal seizures of >10 minutes duration
- Medical emergency
- May occur when awake or asleep but no regaining of consciousness between attacks
- *most uncommon, but most life-threatening
Seizure Diagnostics
Assesment
- Presence of aura, onset, spread, type of movement, body parts involoved, pupil changes and reactivity, duration, loss/LOC, incontinence, behavioral and neuro changes after cessation of sz activity
- Note HA, fever, personality changes
EEG *most important test in determining sz classification
CT head for new onset seizures to r/o brain tumor
Seizure Management
Initial tx is supportive as most sz are self-limiting
- Maintain open airway, nothing in mouth
Parenteral anticonvulsants for rapid cessation of sz
- Benzos- Diazepam 5-10 mg IV (to break & status)
- Lorazepam (ativan) 2-4 mg IV at 1-2 mg/min to break
- Phenytoin (dilantin) loading dose 20mg/kg @ 50mg/min continuous infusion
- Fosphenytoin (cerebyx) Prodrug of dilantin
- Phenobarbitol (Luminol) Used if phenytoin is unresponsive
- Barbituate coma or GA with nueromuscular blockade
Subsequent Seizure Prevention
Maintenance dosage long-acting anti-convulsants
- Carbemazepine
- Phenytoin
- Phenobarbitol
- Valproic acid
- Primidone
- Clonazepam
Titrate dosage
Never abruptly withdraw, taper
Myasthenia Gravis
Autoimmune disorder resulting in reduction of acetylcholine receptors at the neuromuscular junction
- Weakness is worse after exercise and better at rest
- Variable course
- Age 20-40 at onset, incidence peaks in 30’s women, 50-60 for men
- Women> men
Myasthenia Gravis signs and symptoms
- Ptosis
- Diplopia
- Dysarthria
- Dysphagia
- Extremity weakness
- Fatigue
- Respiratory difficulty
- Sensation and DTR WNL
*Visual changes with extremity weakness are characteristic
Myasthenia Gravis Diagnostics
- Antibodies (AchR-ab) found in >85%
- Edrophonium (Tensilon) test differentiate btwn MG and cholinergic crisis (weakness gets better with Tensilon, worse in a cholinergic crisis)
Myasthenia Gravis Management
- Neuro referral
- Acetylcholinesterase ihibitor drugs (pyrostigmine bromide=Prostigmin)
- Immunosupressives
- Plasmapheresis
- Ventilator support in a crisis
Multiple Sclerosis
Autoimmune disorder characterized by numbness, loss of muscle coordination, vision, speech and bladder control issues
- Attacks myelin sheath which controls transmission of nerve signals
- Variable course
- Onset 20-50 years
- More common Western European descent in temperate zones
MS Signs & Symptoms
- Weakness, numbness, tingling or unsteadiness in limb
- Spastic paraparesis
- Diplopia
- Disequilibrium
- Urinary urgency or hesitancy
- Optic atrophy
- Nystagmus (rapid eye movements)
MS Diagnostics
- Multifactorial dx, not on labs alone
- Mild lymphocytosis
- CSF: elevated protein, IgG
- MRI of brain
MS Management
- Neuro referral
- No tx to prevent progression
- Steroids for relapses
- Anti-spasmodics
- Interferron therapy
- Immunosuppressives
- Plasmapheresis
Guillain-Barre
Acute, rapidly progressive form of inflammatory polyneuropahty characterized by demyelinization of peripheral nerves resulting in progressive symmetrical ascending paralysis
- Ususally preceded by suspected viral infection with fever 1-3 weeks prior to onset of BLE muscle weakness
- Flaccid paralysis can occur within 48-72 hours of onset
GB Signs & Symptoms
- Rapidly progressive ascending paralysis
- CN impairment AEB difficulties in speech, swallowing, mastication
- Reflexes hypoactive or absent
- Respiratory muscle impariment possible
GB Diagnostics and Management
Diagnostics
- CSF protein elevated
- CBC: leukocytosis with left shift
- LP, MRI, CT sometimes used in dx
Treatment
- Supportive while myelin regenerates
- Sx recede w/in 2 weeks, resolve w/in 2 years
- Neuro consult
Meningitis
- Should be considered in any patient with fever and neurologic symptoms, especially if history of other infection (PNA) or head trauma
- Acute, bacterial meningitis is a medical emergency
Causes
- Strep pneumoniae, H. Influenze, N. Meningitidis in 80-90% of cases
- Most common in the hospital is Staph Epidermis
Meningitis Signs & Symptoms
- Fever (101-103)
- Severe HA
- N/V
- Nuchal rigidity
- Positive Kernig’s Sign (pain and spasm of hamstring muscles)
- Positive Brudzinski’s Sign (legs flex at hips and knees in response to flexion of the head and neck to the chest)
- Photophobia
- Seizures
Meningitis Diagnostics & Management
Diagnostics
- Lumbar Puncture - Bacterial presentation: CSF cloudy or xanthocrhomic (yellow) with elevated pressure, protein, decreased glucose (bugs eat sugar) and presence of WBC’s
- Viral Presentation-normal to elevated opening pressure, normal protein and glucose, some WBC
- CT head is indicated
Management
- Control S&S, maintain electrolyte balance
- High dose parenteral ATB therapy ASAP for suspected bacterial cases
- Aqueous PCN G, vanc with a third gen cephalosporin until C&S is available, or fluoroquinolones
Head Trauma
- Men< 35 years, accidents leading cause of death
- Over 70% accidents involve head injury
- Leading cause of death in all trauma cases
Monroe-Kellie Doctrine: when 1 content of brain goes up (blood, CSF, Brain tissue), another goes down
S&S:
- Assess: time and place of injury, how it occured, LOC, occurence of a lucid interval (suggests bleed *Epidural hematoma), sz activity, amnesia (indicates severity of blow)
Decompensating pts may show Cushing’s Triad:
- Widening pulse pressure (SBP increases in attempt to maintain CPP (CPP=MAP-ICP))
- Decreased RR
- Decreased HR
Battle’s sign -bruising at mastoid
Raccoon eyes
Otorrhea or Rhinorrhea
Head Trauma Diagnostics/Management
Diagnostics:
- C Spine films all pts
- Skull films and Head CT
Management:
- ABC’s assessed in any significant head trauma or altered LOC
- Stabilization of VS and ongoing Neuro eval
- Neurosurgery consult
Spinal Cord Trauma
- 1/2 of all spinal cord injuries occur above T1
- More common in young males
Four P’s:
- Paralysis
- Paresthesias
- Pain
- Position
Levels of Vertebral Damage
- C4 or above- Quad, may need vent
- C4-C5: Quad, control of head/neck, shoulders, trapezius, elbox flexion
- C5-C6: Quad, some extension of wrist, index finger/ thumb
- C6-C7: Elbow extension, capable of feeding and dressing
- C7-T1: Hand movement
- T1-T2: Para, upper extremity control, no trunk control
- T3-T8: Some trunk control
- T9-T10: Bowel and bladder reflex, moves trunk and upper thigh
- T11-L1: Most leg and foot, ambulation possible
- L1-L2: Lower legs, feet, perineum, bowel, bladder and sexual function if S2-4 nerves involved
- *C=arms and hands, T=trunk
Strength Grades
5/5 normal
4/5 Full ROM against moderate resistance and gravity
3/5 Full ROM against gravity, not against resistance
2/5 Can move but not against gravity (roll, not lift)
1/5 Muscle contracts, no movement of extremity
0/5 Flaccid
Spinal Cord Injury Diagnostics/Management
Diagnostics:
- Spinal XR series
- CT scan, MRI, myelography
Management
- Methylprednisone 30 mg/kg IV bolus followed by infusion of 5.4 mg/kg/hr 23 hours improves neurologic recovery when administered w/in 8 hrs of injury
- Neuro consult
Spinal Cord Injury 2 major complication types by Level
C4 or above- resp compromise
T4-T6 - autonomic dysreflexia, emergency condition (seen in full bladder or annoying type problem like a wrinkled sheet)
- exagerated autonomic response to stimulus
- diaphoresis and flushing above level of injury
- chills and vasoconstriction below injury
- HTN
- Bradycardia
- HA-severe
- Nausea
- Tx -antihypertensives and removal of stimulus
T6 or above: Neurogenic shock
- During transmission of sympathetic impulses, unoppsed parasympathetic stimulation leading to loss of vasomotor tone inducing vasodilation
- Hypovolemia, decreased venous return, decreased cardiac output
- Sympathomimetic vasopressors
Cause of Parkinson’s Dz
Degenerative disorder resulting from insufficient dopamine in the body
- Onset 45-65, idiopathic, equal gender distribution, all ethnic groups
Parkinson’s Signs/Symptoms
Most common are top three:
- Tremor, enhanced by stress
- Rigidity
- Bradykinesia (slow movement)
Additional sx:
- Wooden facies
- Dysphagia
- Drooling, decreased blinking
- Myerson’s sign (tapping over bridge of nose produces sustained blink response)
Parkinson’s Diagnostics/Management
Diagnostics:
- None
Lung problems/infection usually is cause of death
Management
Increase dopamine (If difficulty moving, like feet sticking to flr)
- Carbidopa-Levodopa (Sinemet), Amatadine (Symmetryl), Tolcapone (Tasmar), Pramipexole (Mirapex), Ropinirole (Requip)- all are used in combination, not alone
Anticholinergics (for worsening tremor)
- Benzoropine (Cogentin), Trihexyphenydyl (Artane)
Selegiline (Edepryl) or Depranyl
Drug Abuse/ Alcoholism Pneumonic
C- need to Cut down?
A- people Annoyed you by criticizing your drinking?
G- felt Guilty?
E- need for Eye-opener drink in the morning?
Managment:
- Consult regarding tx and detox
- Therapuetic communication “I’m concerned about alcoholism”, not you have a drinking problem
- Treatable dz
- AA referral, Al-Anon (family) /Ala-Teen
Confusion- Delerium vs Dementia
Delerium: sudden, transient onset of clouded sensorium, occurs at any age, associated with physical stressor
Causes:
- Toxins, alcohol/drugs, trauma, Fecal impaction, poor nutrition, electrolye imbalance, anesthesia
Dementia: Gradual memory loss, not recoverable with decreased intellectual functioning, >60 years of age
Causes:
- Atherosclerosis, neurotransmitter defecits, cortical atrophy, ventricular dilation, loss brain cells, viral, Alzheimer’s
Alzheimer’s
Development of multiple cognitive defects characterized by both memory impairment and:
Aphasia (difficult speech)
Apraxia (Inability to perform previously learned task)
Agnosia (Inability to recognize object)
Inability to plan, organize, sequence and abstract thought
Other findings: limb rigidity, flexion posture, gait disturbance
*Most common cause of dementia
*acetylcholine deficiency
Diagnostics:
Draw labs to r/o other diseases
CT/MRI r/o tumor
Management:
Meds to increase ACTH (acetylcholinesterase inhibitors)
Donazepril (Aricept), Galantamine (Razadyne), Rivastigmine (Exelon)
Referral for counseling
Gerontology Considerations
Increased risk of sleep disorders, delerium, neurodegenerative diseases, falls, loss of independence with ADL’s
Physiologic changes: decreased neurons and neurotransmitters, decreased thermoregulation, peripheral nervous changes, decreased dopamine receptors, increased alpha responses
Impaired muscle strength, sense of touch, increased pain tolerance, slowed motor skills, diminshed balance, temp sensitivity, blunted temp response, slowed cognitive response but not intelligence
Dysarthria
Not able to articulate
Apraxia
Inability to perform a previously known task
Amaurosis Fugax
Ipisilateral, monocular blindness
Time limit for TPA/thrombolytics
3 hours
Want CO2 low in the head?
It causes vasoconstriction to cerebral vessels
CO2 Level should be 35
Cerebral perfusion pressure equation
CPP= MAP-ICP
Keep MAP high 110-130
CCB used to prevent vasospasm in head bleed?
Nimodipine/Nimotop
What is difference between a simple partial and complex partial sz?
Loss of or impaired consciousness
How to differentiate tonic-clonic from complex partial?
Tonic clonic- blue, loss of bladder control, change in LOC but will be POST-ICTAL
Name two out-pt anti-sz drugs
Tegretol and dilantin
Wihch hemisphere presents with left hemiparesis, right visual field changes, spatial disorientation (can’t determine true body postition)
Right hemishpere hemorrhagic stroke
brudzinski sign
head to chest and they curl up knees and hips (like a baby)
Kernig’s sign
Pain and spasms of the hamstring muscles
With fast onset, suspect viral or bacterial meningitis?
Bacterial
Brown sequard syndrome
ipsilateral symptoms, contralateral pain
Raccoon eyes
Basilar skull fx
Lucid interval
Epidural hematoma
(arteries are outside, arterial bleed)
Slow onset, bonk on head, weird behavior, on blood thinner
Subdural hematoma
Cushings triad
1) widening pulse pressure (BP up)
2) decreased HR (vagal stimulation)
3) respiratory rate decreased, irregular
Herniation of brainstem
c 4
breathe no more
On the vent
Quad
Cervical spine
Lumbar
Lower legs
spinal
sexual function
2/5
zero against gravity
are steroids used in spinal cord injury?
yes if within 8 hrs of injury
Methylprednisone 30 mg IV bolus
Which hemisphere hemorrhagic stroke presents with right hemiparesis, aphasia, dysarthria, difficulty reading/writing
Left (dominant) hemisphere
Thromobolytic criteria for ischemic CVA
fibrinoltyic therapy if <3 hrs onset
Goal for ICP with CVA?
Maintain CPP and limit increases in ICP to <20
How to prevent cerebral vasospasm?
Nimodipine (Ca Channel agonist) to counter vasospasm
MAP 110-130 to treat cerebral vasospasm
Which type of seizure is common with cerebral lesions?
Simple partial
Autonomic dysreflexia
Bladder or rectal stim causing HTN or other syndromes
In which disease are steroids contrindicated?
guiliian-barre
Central Cord Syndrome
Hyper extension injury with discord between upper and lower symptoms
Can walk across the room but can’t shake hands
Mini-Mental status exam pneumonic
O rientation to place and time
R egocnition (3 objects)
A ttention (7’s backward)
R ecall (recall the 3 objects 5 min later)
Language
2 identify 2 names of objects
3 Follow 3 step command
R eading a statment and doing it without saying it aloud
W riting a sentence
D rawing a design (copy)
MMMS exam scoring
Max 30
No impairment 24-30
Delerium/Dementia or both: 18-23 mild, 0-7 severe
Hemianopia
1/2 visual field loss
CPP= MAP-ICP
Drug of choice to prevent/counteract vasospasm in CVA?
Nimodipine (CCB)
Eventual capabilities in SCI by level
C4 breathe no more
C1-T1: Quadraplegia, may have use of arms
T1-L1: Paraplegia
T9-L1: May eventually ambulate
L1-L2: bowel and bladder
If S2-S4 involvement, may have sexual dysfunction
Myerson’s sign
Parkinson’s -
tapping over bridge of nose produces sustained blink response
Dementia Pneumonic
D- Drug reaxn
E- Emotional disorder
M- Metabolic/endocrine
E- Eye/ear disorder
N- Nutritional problem
T- Tumors
I- Infxn
A- Atherosclerosis
*Most common cause of dementia
*acetylcholine deficiency
