Neuro Flashcards
Cranial Nerves
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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
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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