Neurology I Flashcards
List some levels of consciousness
Coma
Brain Death
Persistent Vegetative State
Minimally Conscious State
Locked-In Syndrome
1) Define coma
2) What may still be intact?
1) Patient is unarousable and unresponsive > 1 hr
2) Reflexes may still be intact
Do comas have an abrupt or slow onset? Describe.
Either:
1) Abrupt onset: think stroke or hemorrhage
2) Slow onset: mass or structural (brainstem) lesion
What are two causes of coma?
1) Structural lesions
2) Metabolic disturbances
How do assess coma?
ABC’s –treat as necessary
If hypothermic, rewarm and reassess
CMP, blood gases
CT head, CTA brain
Corneal reflex
Pupils
Response to painful stimuli; unilateral vs bilateral?
Oculocephalic reflex
Nystagmus?
Breathing patterns?
As time progresses any other neurologic deficits?
Coma:
1) What does it suggest if corneal reflex is absent unilateral?
2) What if it’s absent bilaterally?
1) Defect of the ipsilateral pons or trigeminal nerve
2) Meds, large pons defect
What should you assess for regarding the pupils when your pt is in a coma? What does each suggest?
1) Horner’s syndrome (what is the triad?)
2) Pinpoint (opioid overdoses)
3) No direct or consensual response to light (CN III)
How do you Tx coma?
1) Support
2) Correct any of the abnormalities found during assessment.
3) Thiamine, dextrose, or naloxone can be given IV without awaiting lab results
What 3 things can you do to Tx coma before labs get back?
Thiamine, dextrose, or naloxone
Define brain death
based on clinical exam
no evidence of forebrain or brainstem function (complete and irreversible)
no sleep-wake cycles
No eye or pupil movement
Apneic
No brainstem reflexes (corneal reflex, pupil response to bright light, pain stimulus, gag reflex)
Cerebral angiogram if needed
True or false: a brain dead pt may be kept on vent for organ donation
True
Vegetative state:
1) What is another name for vegetative state?
2) What can the pt still have/ do?
3) How can the pt appear?
4) What is absent?
5) What can cause it?
unconscious state
can have sleep-wake cycles and other responses or reflexes mediated by the brainstem
May appear awake, but no meaningful activity
no purposeful movement or meaningful speech
though may make sounds
incontinent.
Can be caused by anoxic brain injury or TBI
Minimally conscious
Inconsistent levels of consciousness
Some self-awareness
Basic verbal communication and gestures
Can follow simple commands (wiggle fingers, blink eyes)
Can be temporary or permanent depending on cause
After 12 months, unlikely to have any meaningful recovery
How do you Tx minimally conscious pts?
1) Underlying cause – if able
2) Amantadine
For each cause of coma, describe what the pupils would look like:
1) Toxic and metabolic disorders
2) Midbrain lesion or herniation
3) Pontine lesion
4) Opiate overdose
1) Normal (usually)
2) Unilateral or bilateral “blown” pupils
3) Small, responsive to light bilaterally
4) Pinpoint pupils bilaterally
Describe the capabilities of pts with locked-in syndrome
motor function is absent
sensation and cognition are intact. Fully aware of surroundings
Can still move eyes vertically and hear. pupillary responses are intact
Mute and quadriplegic, but conscious
Locked-in syndrome
1) What typically causes it?
Usually due to infarct in the ventral pons, affecting the corticospinal and corticobulbar tracts. So, the spinal cord and cranial nerves receive no input from the cortex therefore, the patient cannot move. But sensory pathways and arousal systems in brainstem are spared, so patients are aware and able to feel, hear, and understand. Eye movements are spared as their control center is in the rostral midbrain**Note this is different from coma
True or false: pts with locked-in syndrome typically have a poor prognosis
True
What are the 4 As of cognitive impairment?
Aphasia
Agnosia
Apraxia
Amnesia
What are some causes of cognitive impairment?
strokes, tumors, infections, hypoxia, toxins (CO,) head injury, developmental disorders, other neurological diseases
What is aphasia and what causes it?
Inability to express or receive written/verbal communication; damage to Wernicke’s or Broca’s areas
1) Define agnosia
2) What causes it?
3) Give examples
1) Inability to recognize things/people/places
2) Damage to parietal, temporal or occipital lobes
3) Astereognosis, topographic agnosia
1) Define apraxia
2) What can cause it?
1) Disordered skilled movements; can perform, but does so incorrectly
2) Can be widespread or focal cerebral damage
1) Define amnesia
2) List some potential causes
1) Memory loss (recent or new memories)
2) Damage to hippocampus: stressful events, ischemia, h/o migraines, advanced age, injuries, drugs, alcohol, trauma, neurologic conditions
1) What is Electromyography (EMG)?
2) What does it calculate?
3) Is it done bilat or unilat?
1) Nerve conduction study; stimulate nerve and record response of muscles
-Or electrical activity, which is typically tested with needles
2) Calculates the conduction velocity of the
nerve (ms) (sensory and/or motor)
3) Typically done bilat
Electromyography (EMG):
1) What can cause prolonged results?
2) What can cause prolonged or absent results?
1) Demyelination
2) Peripheral neuropathy
1) What is an advantage of EMGs?
2) What are some disadvantages?
1) Sensory studies can help locate lesions either proximal or distal to the dorsal root ganglion.
2) Results easily influenced by outside factors such as limb temp, edema, age, gender, or jewelry
Also, the studies evaluate the more proximal portion of the nerves therefore may assess fingers but not fingertips.
True or false: peripheral neuropathy may be tested with EMG
True
What are some clinical indications for an EMG?
1) Distinguish between peripheral neuropathy from myopathy and motor neuron diseases
2) Distinguish between subclinical (carpal tunnel) and inherited, acquired, axonal, and demyelinating polyneuropathies via changes in amplitude and velocity especially over time.
3) Suspected myasthenia gravis: can test repetitive stimulation of motor nerves
4) After injury can be used to assess for denervation
5) Assess for inflammatory myopathies and muscular dystrophy, neuropathic vs myopathic vs ALS vs radiculopathy, MS, hypercalcemia, acute vs chronic myopathy
1) Where are subdural hematomas?
2) What is it associated with?
3) Who is more prone to SDHs?
4) What is acute SDH usually accompanied by?
5) What does it look like on head CT scans?
1) Between dura and arachnoid meninges (bridging veins)
2) Usually not associated with skull fracture, but rather a result of deceleration injury (MVA) or falls in elderly.
3) Patients with cerebral atrophy (age, EtOH)
4) More severe cerebral injury and increased intracranial pressure.
5) Crescent shaped bright bands that DO NOT CROSS the midline
Subdural hematoma:
1) When does it typically occur?
2) When do Sx occur? What happens to half of pts? Describe
1) Typically occur after head injury (fall, assault, MVA)
2) Symptoms usually occur immediately after injury
-About half of patients will lose consciousness at time of injury
-Others arrive to hospital in a coma
-Some will stay awake and then lose consciousness again if hematoma is growing
Slide 22
Most patients present with ipsilateral pupillary dilation and contralateral hemiparesis
Common history of alcoholism or epilepsy
** check to see if patient on anticoagulants
1) Glasgow Coma Scale measures what?
2) What is mild, moderate, and severe?
1) TBI severity
2) MILD = 13-15
Moderate = 9-12
Severe = < 8
Describe a Subdural Hematoma Evaluation. Incl what needs to be done to protect the pt.
ABCs and mental status, eyes
1) Stabilize patient/correct vitals (O2, fluids) keep BP at age-appropriate target
2) Detailed history and exam, baseline neuro eval, Assess GCS (<8 intubate) and treat as needed
3) Evaluate severity of head injury, assess for spinal fracture and any other injuries
4) Protect c-spine. Once stable, CT head
5) Eval for HA, n/v seizure activity, confusion, recent drug or alcohol usage, unilateral deficits
7) Detailed inspection/palpation for skull fractures, CSF leakage (“halo” of CSF around bloody discharge on white cloth/coffee filter)
What do you need to closely monitor in subdural hematoma pts?
Ongoing neuro checks, eyes and pupils, nystagmus
How do you test for subdural hematoma?
“Halo” of CSF around bloody discharge on white cloth/coffee filter
What will a CT of a pt with a subdural hematoma reveal?
Crescent-shaped bleed
What are 3 types of primary headaches?
Cluster, migraine, tension
What is your job as a PA when a pt presents with a headache?
Decide if “benign” headache vs. headache with dangerous neurologic or systemic pathology (Red Flag)
Differentiate between primary and secondary HAs
Primary HA - benign, do not have a separate underlying etiology that requires further evaluation
Secondary HA – some secondary HA can be life-threatening, caused by underlying processes, such as medication overuse, infection, head trauma, or intracranial bleeding
What are most headaches assessed in primary care?
Primary
Primary headaches are benign; how common is each type?
Tension type ~ 46-78%
Migraine ~ 14-16%
Cluster< 1%
What are some causes of secondary headaches?
SAH, head trauma, infection, tumors, giant cell arteritis, etc.
Most headache diagnoses are based primarily on which of the following?
A. history
B. exam findings
C. laboratory testing
D. imaging
A. history
Headaches
Exam findings are usually normal at time of evaluation
Laboratory and imaging utility - r/o secondary causes of headaches
Describe cluster headaches
-Episodic, severe, unilateral, rapid onset, periorbital pain daily for several weeks.
-Can awake pt at night, last 15 min- 3 hr, 1-8x/d x 4-8 weeks.
-Spontaneous remission then recur weeks to months later
Cluster headaches:
1) Who are they more common in?
2) What are some associated symptoms? Are Sxs unilateral or bilateral?
3) What are some triggers?
1) M»F
2) Assoc symptoms: ipsilateral nasal congestion, rhinorrhea, lacrimation, red eye or Horner’s syndrome. Patient is agitated and restless, paces
3) unknown, typically no FH of HA, considered a trigeminal autonomic cephalgia, activation of posterior hypothalamus
Cluster headaches:
1) How to rule out DDxs?
2) Epidemiology?
3) Age range?
4) Main Tx?
1) Unilateral periorbital pain with ipsilateral autonomic symptoms
2) Much less common than migraines, prevalence in males = 0.4-1%
3) Age 20-60
4) High flow O2 via non-rebreather mask
Describe Txs for cluster headaches
Tx: high flow O2 via non-rebreather mask
Injectable sumatriptan 2-6 mg (max 12 mg/d)
Short term high dose steroids
High doses of verapamil
d/c smoking, alcohol
Migraine headaches:
1) What are the two main kinds?
2) How long does it last without treatment?
3) How many attacks?
1) With (20%) or without (80%) aura
4-72 hrs w/o tx
At least 5 attacks
Migraines:
1) Includes >=2 of what pain characteristics?
2) And >=1 of what?
1) Unilateral
Pulsating
Mod-sev intensity
Worsened by or causes avoidance of routine physical activity
2) Nausea or vomiting
Photo or phonophobia
Migraine Headaches with aura can also include visual or sensory symptoms; give examples
1) Flickering lights
2) Blind spots
3) Loss of vision
4) Feeling of pins and needles
5) Numbness
6) Difficulty producing speech
7) Aura lasts 5min-1 hr prior to HA
8) Neck pain
9) Lacrimation
10) Rhinorrhea
Migraine headaches:
1) What is the pathophys?
2) What is the etiology?
3) What is the epidemiology?
1) Neuropeptide release leads to neurogenic inflammation of meningeal vessels and trigeminal sensory fibers; hyperexcitable neuro cortex
2) Unknown, thought to be familial and genetic
3) F»M 18% of women experience migraines (only ½ are diagnosed) 1 in 7 people globally; more common in western hemisphere. Migraines increase as a patient ages to 40, then begin to diminish
Acute migraine 4th most common reason for ER, ~ 53% present to primary care
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Less common than Tension HA, more disabling – affects ADL’s
Most common cause of disabling HA’s and most common cause for medical visit due to HA (94%)
1) What are some potential triggers for migraines?
2) What are some DDxs for migraines?
1) Triggers: over or under sleep, caffeine, stress, dehydration, 5C’s (cheese, Chocolate, coffee, coke, citrus fruits,) menstrual cycle, pungent odors
DDx: cerebral hemorrhage, tumor, infections, meningitis, other types of HA’s, stroke
True or false: Migraine patients will have normal neuro exam.
True
Migraines:
1) What are the goals of Txs?
2) How to Tx acute cases?
3) What else can be used in pts with n/v?
1)eliminate pain and assoc symptoms without increasing disability. (ex/ avoid sedation;) early intervention; avoid known triggers
acute – early use of high dose NSAIDs (though must weigh risks/benefits)
Triptans** preferred nasal sprays or injections can be used in patients with n/v
CONTRAINDICATED in CAD and cerebrovascular disease
slide 40 migraines
acute – early use of high dose NSAIDs (though must weigh risks/benefits)
Triptans** preferred nasal sprays or injections can be used in patients with n/v
CONTRAINDICATED in CAD and cerebrovascular disease
Combo therapy highest yield *NSAIDs + triptans) can also add metoclopramide or Compazine in pts with n/v as well
1) What should you avoid in migraine pts?
2) When is botox approved?
3) What can be used to reduce occurrence? What is the downside of this Tx?
AVOID OPIOIDS few opioid receptors in trigeminovascular neurons, they are proinflammatory, risk of overuse
Botox approved for migraines>15 days of HA/mo
Corticosteroids can be used to reduce occurrence, but do not work acutely and have high SE profile
Migraines:
1) When can prophylactic Tx be used? Give examples of this Tx
2) What are some new treatments?
1) In patients experiencing > 6-8 migraines/mo [ex/ propranolol (can worsen depression,) amitriptyline, verapamil (can trigger HA’s,) or gabapentin]
2) Monoclonal antibodies
Migraines:
1) What can help besides traditional Tx?
2) What can help menstrual migraines?
3) What can relieve some migraines?
4) What can trigger migraines?
1) Alternative therapies (ex/ acupuncture, hypnosis)
2) Estrogen supplements for menstrual migraines
3) Pregnancy can relieve some migraines few therapies are approved for use in pregnancy
4) Migraine patients often have many comorbidities including depression, bipolar, mania, anxiety, however antidepressants can trigger migraines in some patients
Tension-Type Headaches (TTH): How is it defined? How long does it last?
> = 10 “band-like” episodes of pain occurring on 1 d/mo
HA lasts 30 min to 7 days
Tension-Type Headaches (TTH): pts must have at least two of what pain characteristics?
Bilateral location
Pressing or tightening (non-pulsating) quality
Mild-moderate intensity
Not aggravated by routine physical activity
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Photo OR phono phobia, but not both; no n/v
45
Tension headache epidemiology
Most common form of HA’s –
1/3 – ¾ of adults experience tension HAs
F>M, age 30’s – 40’s, reduce with age
Found worldwide though prevalence varies greatly based on age, population studied and survey methodologies
Tension headache etiology
contraction of neck and scalp muscles due to
Mental tension, fatigue, missed meals, stress, noise
As well as heightened sensitivity of pain pathways in the CNS
NO focal neuro deficits
What is the most common type of headache seen in primary care?
A. cluster
B. migraine
C. tension
D. post traumatic
C. tension
What are the Low-risk HA criteria?
1) Age < 30 years
2) Features typical of primary headaches
3) History of similar previous HA (not “worst headache ever”)
4) Consistent headache symptoms…not evolving quickly
5) **Normal neurological exam
6) No high-risk comorbid conditions
7) No new concerning historical or exam findings
Severe headaches:
1) What are they? Where are they seen?
2) What mnemonic can help avoid missing a life-threatening diagnosis among the more common primary headaches?
1) May be life-threatening
Rarely present to primary care clinics…..~ 1%
SNNOOPPPP
What are some DDxs for severe headaches?
1) Intracranial disorder, infection or non-vascular condition
2) SAH
3) Giant cell arteritis, cervical or intracranial lesion
What is the SNNOOPPPP mnemonic for red flag Sx in pts with headaches?
Systemic symptoms – fever, rash, myalgia, weight loss, HTN
Neoplasm – history of cancer,
Brain primary or mets
Neurologic deficit or dysfunction – focal exam, Sz, AMS/cognitive changes
Onset abrupt (thunderclap HA)
Older patient (> 50 y/o)
Pattern change or new type of HA
Papilledema
Painful eye
Pregnancy
What are some H&P findings of severe headaches most associated with significant intracranial pathology
1) HA that do not meet any primary HA criteria, HA with aura, abnormal neuro exam, worse with exertion, or Valsalva
2) Primary HA onset after 50 y/o is uncommon
3) > 65 y/o is concerning for serious secondary cause….Giant cell arteritis if > 50 y/o
4) Brain cancer risk in a patient with a HA w/out a previous h/o cancer is < 0.1%; lung, melanoma and breast (LaMB) highest risk for moving to brain
1) What are some Sxs of giant cell arteritis?
2) What cancers can easily spread to the brain?
1) Fever, scalp tenderness overlying temple, jaw claudication (pain with chewing)
2) Lung, melanoma and breast (LaMB) highest risk for mets to brain
1) What headaches rarely need neuroimaging?
2) How common is it for migraines to have significant IC pathology?
3) What likely suggests underlying cause?
1) Stable primary headaches
2) Migraine HA ~< 0.2% prevalence of significant IC pathology
3) HA + abnormal neuro exam
Dizziness
1) Define dizziness
2) What is the pathophys?
3) What is the epidemiology?
1) Altered sense of balance, may be lightheaded or presyncopal
2) Vasovagal reaction, postural hypotension, hypoperfusion of CNS possibly from CV pathology
3) One of the most common complaints in medicine, 20-30% of general population
What is the etiology of dizziness?
Pathologies in any of the following pathways:
1) Visual
2) Proprioceptive
3) Vestibular
What are some DDxs for dizziness?
1) Vertigo (head or room is spinning,)
2) Lightheadedness, syncope, meds
3) Imbalance, anemia
4) Meniere’s Dz, psychophysiological disorders
5) Vestibular neuritis, hypoglycemia
6) Whiplash injury
7) Migraine, tumor, hypothyroidism
8) DM, cardiac arrythmias, orthostatic hypotension,
Dizziness: What might you see on PE? What should your PE include?
1) +nystagmus, no focal neuro deficits
2) Need audiologic eval
3) Test proprioception and vestibular system
Dizziness:
1) How do you Tx?
2) What are last resort Txs?
1) Treat any underlying disorders, vestibular suppressant (meclizine), antiemetics, vestibular rehab
2) Intratympanic injections, surgery
Vertigo:
1) Define it
2) What is the pathophys?
3) What is the etiology?
1) Spinning sensation +/- n/v
2) Semicircular canal abnormality or nerves thereof
3) Spinning in circles, meds; peripheral»_space; central
Vertigo:
1) What are some common peripheral causes?
2) What is the epidemiology?
1) BPPV, vestibular neuritis, Meniere dz ; common central: vascular lesions, migraines, lesions of brainstem or cerebellum
2) Not too frequent. Lifetime prevalence <8%
Vertigo:
1) What are some DDxs? Explain
2) How do you Tx?
1) Vertigo is a symptom not a diagnosis, therefore if a patient presents with vertigo, your DDx would include any of the peripheral causes + most other CNS diseases: MS, tumors, acoustic neuroma, meds, OM, TIA, seizures, disembarkment syndrome
2) Tx: underlying cause
Cranial Nerve Palsies:
1) What are they?
2) Etiology?
3) How to Tx?
4) Give some examples of CN palsies
1) Dysfunction of cranial motor nerves, can include pain, vertigo, hearing loss, weakness, numbness, tingling or paralysis (facial drooping)
Etiology – trauma, compression (tumor, bleed, infection,) DM, HTN, stroke
3) Decompression surgery, B vitamins 6, 12, correct underlying cause if able
Ex/ Bells Palsy, ophthalmologic palsies
Bells Palsy:
1) Define this condition
2) What is NOT present w this?
3) What is the pathophys?
4) Epidemiology?
Sudden onset of facial palsy CN VII (affects forehead,) with impaired taste, pain near the ear may be present at the start for a couple of days
** NO OTHER neuro deficits**
Pathophys: inflammation of the facial nerve near the stylomastoid foramen
Epidemiology - lifetime risk in 1 in 60; 40,000 new cases/yr; pregnant women and DM more common
Ballsy Palsy:
1) Etiology?
2) DDxs?
1) Etiology: idiopathic, possible HSV or VZV
2) Stroke, central brain lesion
How to Tx bells palsy?
60% spontaneously resolve
1) Prednisone 60 mg PO QD x 5d followed by 5d taper increases the chance of complete recovery by 1 yr
2) Acyclovir or Valacyclovir if presence of herpetic vesicles in EACs
3) Lubricating eye drops
Bulbar palsy:
1) What is it?
2) What are some clinical features?
3) What is the pathophys?
1) Symptoms that can occur due to damage to the lower cranial nerves (CN 9-12).
2) Range from difficulty swallowing and a lack of a gag reflex to inability to articulate words and excessive drooling.
3) Corticobulbar disease affecting upper motor neurons
Bulbar palsy:
1) Epidemiology?
2) Etiology?
3) DDxs?
1) Very rare;1 in 100,000 in ALS patients
2) Commonly caused by a brainstem stroke/tumor, viruses
3) Genetic dystrophies, Hodgkin’s disease, West Nile infection, ALS
How to Tx bulbar palsy?
1) Treat underlying disorder
2) Refer to neurology
3) Riluzole PO BID, Edaravone > meds not on exam
What are 3 closed head injuries?
1) Concussion
2) Post concussion syndrome
3) Traumatic brain injury (TBI)
