Neurological Flashcards
Trochlear (4)
Down and inward eye movement;motor
Name the cranial nerves in order
Oh- Olfactor
Oh- Optic
Oh- Oculomotor
To- Trochlear
Touch- Trigenimal
And- Abducens
Feel- Facial
Very- Vestibulocochlear (Assoustic)
Good- Glossopharyneal
Velvet- Vagus
Ah- Accessory (Spinal Accessory)
Ha- Hypoglossal
Olfactory nerve (1)
Smell; Sensory
Optic (2)
Vision;Sensory
Oculomotor (3)
Most extraocular movements, opeing eyelids, pupillary constriction;Motor
Trigenimal (5)
Muscles of mastication, sensation of face, scalp, cornea, mucus membranes and nose;both sensory and motor.
Abducens (6)
Lateral eye movement;motor
Facial (7)
Move face, puff cheeks, close mouth and eyes, taste, saliva, and tear secretion;Both sensory and motor.
Vestibulochoclear (accoustic) (9)
Hearing and equilibrium;sensory
Vagus (10)
Talking, swallowing, general sensation from the carotid body, carotid reflex;both sensory and motor
Accessory (spinal accessory) (11)
Movement of trapezius and sternomastoic muscles (shrug shoulders);motor.
Hypoglossal (12)
Moves the tongue;motor
Type of cranial nerve;motor, sensory or both
Some- 1, sensory
Say- 2, sensory
Marry- 3, motor
Money- 4, motor
But - 5, both
My- 6, motor
Brother- 7, both
Says- 8, sensory
Big- 9, both
Boobs- 10, both
Matter- 11, motor
Most- 12, motor
Mini mental status exam (ORArL 2,3, RWD)
- Orientation to place AND time
- Recognition (repeat three objects ex orange, dog pencil)
- Attention (count back from 100 by 7’s)
- recall (ask to recall three objects 5 minutes later)
- Language
- 2 objects identified (ex clock and chair)
- 3 step command followed (ex take this paper in your right hand, fold it in half and place it on the floor)
- Reading (ex read this statement to yourself, do exactly what it says but do not say it aloud “close your eyes.”)
- Writing (ex write a sentence)
- Drawing (ex copy a design)
Max 30
No cognitive impairment: 24-30
Delirium/dementia: 0-17 (severe impairment), 18-23 (mild impairment)
Seizures
A variety of paroxysmal events occuring as a result of abnormal electrical activity in cerebral neurons.
The international classifiction of seizures is based on mode of seizure onset and spread
Partial seizures (focal or local)
Simple Partial and Complex partial
Simple partial seizure
-Common with cerebral lesions
-NO loss of consciousness
-Rarely lasts more than a minute
-Motor symptoms often start in single muscle group and spread to entire side of body.
-Paresthesia, flashing lights, vocalizations and hallucinations are common.
Complex partial seizure
Any simple partial seizure followed by an impaired level of consciousness
-May have aura, staring, or automatisms such as lip smacking or picking at clothing.
Generalized seizures
Absence (petit mal)
Tonic-clonic (grand mal)
Absence (petit mal) seizures
Sudden arrest of motor activity with blank stare
-Common in children/adolescnce (teachers find it)
-Begins and ends suddenly.
“Absent for awhile”
Tonic-clonic (grand mal) seizures
Begins with tonic contractions (repetitive involuntary contractions of muscle), loss of consiousness, then clonic contractions (maintained involuntary contractions of muscle).
-May have aura
-Usually lasts 2-5 minutes
-Incontinence may occur
-Followed by postictal period
Status epilepticus
A seizure that lasts longer than 5 minutes, or having more than 1 seizure within a 5 minute period without returning to a normal LOC
-Medical emergency
-May occur when the patient is awake or asleep, but the patient never regains consciouness between attacks.
-Most uncommon, but most life threatening.
Autonomic dysreflexia
An emergency clinial condition caused by exaggerated autonomic response to a stimulus.
HTN emergency in pts with injury above T6
Occurs later in the course, days to weeks after injury.
S/S:
-diaphoresis and flushing ABOVE the level of injury.
- Chills and severe vasoconstriction BELOW the level of injury.
- HTN, bradycardia, HA, nausea
TX: Remove stimulus and antihypertensives
Brown sequard syndrome
Caused by damage to one half of the spinal cord.
S/S:
-Same sided (ipsilateral) motor neuron paralysis and loss of prorioception
-Opposite sided (contralateral) loss of pain and temp
TX: MRI and steroids
Phases of seizures
Stabilization phase (0-5min)
Initial therapy phase (5-20min)
Second therapy phase (20-40min)
Third therapy phase (40-60min)
Stabilization phase management (0-5 min)
-Stabilize patient (ABCs)
-Time seizure from onset
-FSBS: <60 treat with 100mg thiamine and amp of D50
Initial therapy phase management (5-20 min)
Choose one:
-IM versed (10mg >40kg; 5mg<40kg) OR
-IV ativan (.1mg/kg; max 4mg may repeat once) OR
-IV diazepam (0.15-0.2mg/kg; max 10mg may repeat once)
If none are available then choose one of these:
-IV phenobarbital (15mg/kg) OR
-Rectal diazepam (.2-.5mg/kg, max 20mg) OR
-Intranasal midazolam, buccal midazolam
Secondary therapy phase management (20-40min)
Choose one of the following as a single dose:
-IV fosphenytoin (20PE/kg; max 1500PR) OR
-IV valporic acid (40mg/kg; max 3000mg) OR
-IV keppra ( 60mg/kg; max 4500mg)
If none are vailable:
-IV phenobarbital (15mg/kg), last ditch effort
NOTE: there is no evidence based prefered choice
Third therapy phase management (40-60min)
Repeat second line therapy OR
Anesthetic dose (with continuous EEG monitoring):
-Thiopental
-Versed
-Pentobarbital
-Propofol
NOTE: there is no evicence based preferred choice
Transient Ischemic Attack (TIA)
Periods of acute cerebral insufficiency lasting <1hour without any residual deficits.
Ischemic strokes are more common (80%) than hemorrhagic strokes.
Causes/geneal concepts:
-Ischemia due to atherosclerosis, thrombus, arterial occlusion, embolus, intracerebral hemorrhage OR
-Cardio-embolic events such as A-fib, MI, endocarditis, valve disease
-TIA is indicative of impending stroke
-Approx 1/3 of pts with TIA experience cerebral infarction within 5 years.
S/S:
-Altered vision: ipsilateral monocular blindness (known as amaurosis fugax); homonymous hemianopia (half vision).
-Altered speech: Transient aphasia
-Motor impairment: Paresthesia of contralateral arm, leg, or face.
-Sensory deficits
-Cognitive and behavioral abnormalities
-Dysphagia
-Vertigo
-Nystagmus
TIA classifications
Vertebrobasilar
Carotid
Vertebrobasilar: Occurs as a result of inadequate blood flow from vertebral arteries (brainstem, cranial nerve impairment)
-Vertigo, ataxia, dizziness, visual field deficits, weakness, confusion.
Carotid: Occurs from carotid stenosis
-Aphasia, dysarthria, altered LOC, weakness, numbness.
Lab/diagnostics of TIA
- CT scan (priority) is best in distinguishing between ischemic, hemorrhage and tumor.
- MRI is better than CT in detecting ischemic infarcts (may be done later)
- Electrocardiogram (workup)
- Echocardiogram (workup)
- Carotid doppler and ultrasonography
- Cerebral angiography (may be done later in ischemic infarcts)
Management of TIA
- First few days in hospital pt is on aspirin and clopidogrel and DC’d on only one.
- Assess for HTN (#1 cause of HF)
- Carotid Endarterectomy decreases the risk of stroke and death in pts with recent TIAs, pts that need them:
-Symptomatic low-risk surgical pts with 50-90% stenosis AND
-Asymptomatic pts with >70-99% stenosis.
Cerebrovascular accident (CVA infarct and hemorrhagic)
The rapid onset of neurological deficits lasting longer than 24 hours, the 5th leading cause of death in the U.S.
Caused by:
-Atherosclerotic changes
-Chronic hypertension
-Trauma
-Aneurysm
-Arteriovenous malformation
-Tumor
S/S of ischemic and hemorrhagic CVA
CVA infarct can produce subtle, progressive or sudden neurologic deficits:
-Changes in LOC, motor weakness or paralysis, visual alterations, changes in vital signs.
Hemorrhagic CVA usually present with acute onset of focal neurologic deficits.
-Signs of sudden increase ICP including altered mentation, headache and vomiting are present when the hemorrhage is extensive.
-With left dominant hemisphere involvement, you’ll see right hemiparesis, aphasia, dysarthria, difficulty reading/writing.
-With right (non dominant) hemisphere involvement, you’ll see left hemiparesis, right visual field changes, spatial disorientation.
Lab/diagnostics of CVA
Large vessel stroke workup with:
-Telemetry
-TEE with bubble study
-Carotid imaging (US, CTA, MRA, angio)
-Intracranial imaging (CTA, MRA, angio)
Lumbar puncture may be performed if the pt has a grade 1 or 2 aneurysm to detect blood in CSF
-LP contraindicated with large bleeds as brain stem herniation can be induced with rapid decompression of the subarachnoid space.
Management of CVA
Assess time of onset/time last seen normal
-Up to 4.5 hrs can do fibrinolytic therapy with tPA
-Up to 6 hours can do mechanical embolectomy for all
Up to 24 hours can do mechanical embolectomy for some
ICP knowledge
3 H’s of ICP:
-Hypotension
-Hypoxemia
-Hypercapnia
Nimodipine, a calcium channel antaognis, helps to counter vasospasms by preventing calcium from entering smooth muscle cells and causing contraction.
Want <20
Lab/diagnostics of seizures
Seizure assessment includes the following:
-Presence of aura, spread, type of movement, body parts involved, pupil changes and reactivity, duration, loss/level of consciousness, incontinence, behavioral and neurological changes after cessation of seizure activity.
EEG is the most important test in determining seizure classification.
CT of the head is indicated for all new onset seizures.
Subsequent seizure prevention
Maintenance doses of long acting anticonvulsants
-Carbamazepine, ethosuximide, phenobarbital, phenytoin, primidone, valporic acid
Dosages should be titrated
D/C should be tapered and never abruptly withdrawn.
Myasthenia Gravis
Autoimmune disorder resulting in the reduction of the number of acetylcholine receptor sites at the neuromuscluar junction.
Weakness is typically worse after exercise and better after rest.
Wariable clinical could with remissions and exacerbations.
Most commonly occurs in women
S/S of Myasthenia gravis
- Ptosis (droopy eyelid)
- Diplopia (double vision)
- Dysarthria (difficulty speaking)
- Dysphagia
- Extreme weakness
- Fatigue
- Respiratory difficulty
- Sensory modalities and DTRs are normal
Lab/diagnostics of myasthenia gravis
Antibodies to acetylcholine receptors (AchR-ab) are found in the serum of ~85% of pts.
Management of myasthenia gravis
- Neurology referral
- Anticholinesterase drugs block the hydrolysis of acetylcholine and are used to symptomatic improvement
- -Pyridostigmine bromide
- Immunosuppresants
- Plasmapheresis
- Ventilator support may be needed during a crisis.
Multiple sclerosis
Autoimmune disease marked by numbness, weakness, loss of muscle coordination and problems with vision, speech and bladder control.
The bodys immune system attacks the myelin sheat, a key substance that serves as a nerve insulator and helps in the transmission of nerve signals.
Variable clinical course with remissions and exacerbations.
More common in persons of Western European descent, living in temperate zones.
S/S of multiple sclerosis
- Weakness, numbness, tingling or unsteadiness in a limb–may progress to all limbs.
- Spastic paraparesis
- Diplopia
- Disequilibrium
- Urinary urgency or hesitancy
- Optic atrophy
- Nystagmus
Labs/diagnostics for multiple sclerosis
- MRI of brain is most specific test
- Definitive diagnosis can never be based solely on lab findings.
- Mild lymphocytosis common
- Slightly elevated protein in CSF
- Elevated CSF IgG
Management of multiple sclerosis
No treatment to prevent progression of the disease–neurology consult.
Recovery from acute relapses hastened by steroids
Antispasmodics
Interferon therapy
Immunosuppressive therapy
Plasmapheresis
Guillain-Barre Syndrome
An acute, usually rapidly progressive form of inflammatory polyneuropathy characterized by demyelination of peripheral nerves resulting in progressive symmetrical ascending paralysis.
Cause is unknown but usually preceded by a suspected viral infection accompanied by fever 1-3 weeks before the onset of acute bilateral muscle weakness in lower extremities.
Flaccid paralysis can result within 48-72 hours.
Males more commonluy affected
S/S of Guillian-barre syndrome
Typical presentation is a rapidly progressive ascending paralysis
Cranial nerve impairment, as evidence by difficulties in speech, swallowing and mastication can occur.
Reflexes are usually hypoactive or absent
Impairment of the muscles of respiration occur as paralysis ascends.
Lab/diagnostics of guillian barre syndrome
CSF protein is usually elevated, especially immunoglobulin G.
CBC, leukocytosis with a shift is seen early.
LP, MRI, CT are sometimes used in aiding diagnosis.
Management of gullian barre syndrome
Treatment is supportive while myelin is regenerated
Symptoms begin to recede within 2 weeks with recovery in 2 years
Neurologist consult
Meningitis
Meningitis should be considered in any patient with fever and neurologic symptoms, especially if there is a history of other infections (pna) or head trauma)
Acute bacterial meningitis is a medical emergency.
Streptococcus pneumoniae most common pathogen
Hemophilus influenzea or neisseria meningitidis
S/S of meningitis
- Fever
- Severe HA
- N/V
- Nuchal rigidity
- Positive kernigs sign: Pain and spasms of hamstring muscles after flexing knee
- Positive Brudzinski’s sign: Legs flex at both the hips and knees in response to flexion of the head and neck to the chest.
- Photophobia
- Seizures
Lab/diagnostics of meningitis
CT of the head is indicated first to rule out bleed or other problem.
LP should be performed as soon as diagnosis is suspected
- Bacterial CSF:
-Cloudy or xanthochromic (yellow in color)
-Elevated pressures
-Elevated proteins
-Decreased glucose
-Presence of WBCs - Viral CSF
-Clear
-Normal pressures
-Normal protein
-Normal glucose
-WBC present
Management of meningitis
Treatment based on age
<50: Vancomycin plus ceftriaxone
>50: Vancomycin plus amoxicillin plus ceftriaxone
Traumatic brain injury (TBI)
An alteration in brain function, or other evidence of brain pathology that is caused by an external force.
Monroe-Kellie Doctrine
When one of the contents of the skull (blood, brain, CSF) increases, another must decrease to compensate and maintain normal ICP.
Epidural hematoma
Bleeding into the epidural space between the skull and the dura mater.
Caused by rupture of the middle meningeal artery.
CT scan shows lens shaped that does not cross suture line.
Generally causes brief loss of consciousness with lucid intervals
Subdural hematoma
Most commonly caused by tearing of bridgning veins, causing bleeding between dura mater and arachnoid mater.
Develops over minutes to hours.
S/S of TBI
Assess:
-Time and place of injury, how the event occurred, onset of symptoms, LOC, occurence of lucid interval, seizure activity associated with event, whether amnesia occurred afterward (indicative of severity of blow)
Decompensating pts may show cushings triade
-Bradycardia
-Decreased RR
-Widening pulse pressure
Battles sign: Brusing behind ear at mastoid process
Racoon eyes: Basilar skull fracture
Otorrhea or rhinorrhea
Complete SCI
Results in absence of sensory and voluntary motor function below the level of injury.
Incomple SCI
Consists of:
* Anterior cord syndrome
* Posterior cord syndrome
* Central cord syndrome
* Brown sequard syndrome
* Cauda equina syndrome
Anterior cord syndrome vs posterior cord syndrome
Anterior: Disruption of blood flow through the anterioir spinal artery.
-Weakness or paralysis with loss of sense or pain and temp.
-Propioception and vibration intact
They’re opposite
Posterior: Disruption of blood flow through the posterior column.
-Decrease in touch propioception and vibration below the level of injury.
-Motor, pain and light touch sensation preserved.
Central cord syndrome
Hyperextension injuries with stretching of the cord and subsequent hemorrhaging in the center of the cord.
-Occurs almost exclusively in the cervical spine.
-Greater motor loss and sensation in the upper extremities than in the lower extremities because the upper extremities are comtrolled by the central portion of the cord.
Cauda equina syndrome
Not a true spinal cord injury but spinal fracture to the thoracic and lumbar levels can cause injury to nerves in the cauda equina.
-Presentation highly variable depending on level of injury.
-Asymmetric weakness or complete paralysis of lower extremities with atleast partial preservation of sensation.
-Pain is often severe and asymmetrical
-Patellar and achilles reflexes absent
-Sphincter disturbances
-Treatment is MRI, steroids and emergent surgery for decompression.
Spinal cord injury levels of function
- C4 and above=respiratory dysfunction
- C4-C5= able to shrug shoulders and flex elbows.
- C5-C6=Diaphragm is intact although paralysis of intercostal and abdominal muscles.
- C6-C7=Elbow extension
- C7-T1=hand movement
- T1-T2=Paraplegic, able to control upper but not lower.
- T3-T8=some trunk control
- T9-T10=Can move trunk and upper thigh
- T11-L1=Ambulation possible
Parkinsons Disease
A degenerative disorder as a result of insufficient amounts of dopamine in the body.
Dopamine deficieny
Wont get any better, we just try to prevent it from getting worse.
Unknown cause, more common in men 45-65 yrs
S/S of parkinsons disease
Trio of findings in all PD pts:
* Tremor- slow, most conspicuous at rest, may be enhanced by stress.
* Rigidity (cogwheel)- robot like movement
* Bradykinesia- slow movement
Other:
Wooden facies, impaired swallowing, drooling, decreased blinking.
Myerson’s sign
Myersons sign
A PD sign
Repititive tapping over the bridge of the nose produces a sustained blink response (glabellar reflex)
Lab/Diagnostics of PD
None, it’s a diagnosis of exclusion
Management of PD
- Carbidopa-levodopa- increases dopamine in the body.
- Dopamine agonists (mimic dopamine):
-Pramipexole
-Ropinirole
-Rotigotine - MAO-B inhibitors, prevent the breakdown of dopamine.
-Selegiline
-Rasagiline
-Safinamide
Delirium
Sudden, transiet onset of clouded sensorium associated with a physical stressor. Reversible.
Can also be caused by:
Toxins, alcohol/drugs, trauma, impactions in the elderly, poor nutrition, electrolyte imbalances, anesthesia.
Dementia
Now called neurocognitive disorder
Gradual memory loss with decreased intellectual functioning usually occurring over the age of 60yrs.
Causes include:
Atherosclerosis, neurotransmitter deficits, cortical atrophy, ventricular dilation, loss of brain cells, possible viral causes and alzheimers (most common form)
Make sure to rule out other diseases
Alzheimers disease
The development of multiple cognitive defects characterized by both memory impairment AND one or more of the following:
-Aphasia (difficulty with speech)
-Apraxia (inability to perform a previously learned task)
-Agnosia (Inability to recognize an object)
-Inability to plan, organize, sequence and make abstract difference.
Caused by an acetylcholine deficiency
Labs/diagnostics of Alzheimers disease
Diagnosis of exclusion although want to rule out other possible causes of confusion such as CBC, CMP, VDRL, liver function etc.
Management of alzheimers disease
Neuro consult
* Cholinesterase inhibitors (increases availability of acetylcholine)
-Donepezil (used in all stages of AD)
-Galantamine (Used in mild-moderate)
-Rivastigmine (Used in mild-moderate)
- N-methyl D Aspartate (NMDA) antagonist:
-Memantine (moderate to severe disease) - Combine preparations:
-Memantine and donepezil (Namzaric) (moderate to severe disease)
CAGE mneumonic screenign test
If pt asks yeas to 2 or more of these then more questions should be asked.
Screens alchol use disorder
C- Have you ever fel you need to CUT down on your drinking?
A- Have people ANNOYED you by criticizing your drinking?
G- Have you ever felt GUILTY about your drinking?
E- Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover? EYE-OPENER
Horner’s syndrome
Affects the face and eye on one side of body due to disruption of nerve pathways.
S/S:
Ptosis, miosis and anhidrosis which is reduced sweat secretion on one side of body/face.
Get an MRA of the neck/head to rule out carotid dissection.
