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
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Say
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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
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