Neuro Flashcards
Valproic acid: potential adverse effects
BLACK BOX WARNINGS: pancreatitis, hepatotoxicity, fetal risk
phenytoin: potential adverse effects
gingival hyperplasia
Ototoxic meds
furosemide
erythromycin
ibuprofen
Sensorineural hearing loss is due to problems with which part of the ear?
The inner ear: Cochlea (organ of hearing), vestibular labyrinth (organ of balance)
Auditory nerve (CN VIII) or its central pathways
Conductive hearing loss is to due to problems with which part of the ear?
Outer ear: pinna, external ear canal
Middle ear: Tympanic membrane, ossicular chain (malleus, incus, stapes), and middle ear space
Weber test
Distinguishes between conductive and sensorineural hearing loss
-conductive: sound lateralizes to affected side
-sensorineural: sound lateralizes to contralateral side
Rinne test
Tests cranial nerve VIII
Evaluates conductive hearing loss
Strike a tuning fork and place it on the mastoid process
Normal: AC = 2x BC
Hearing loss: BC > AC
frontotemporal dementia: presentation
disruptions in personality and social conduct
may have primary language disorder
Lewy Body dementia: management
Medications can be used to treat agitation, hallucinations, and improve cognition or alertness, but do not decrease the rate of cognitive decline
Acetylcholinesterase inhibitors: 1st line
-donezpil, galantamine
If ineffective, atypical neuroleptics
-clozapine, quetiapine, aripiprazole
Lewy Body dementia
progressive degenerative dementia
most frequently characterized with bradykinesia and rigidity
-memory deficits
-reduced alertness
-visual hallucinations
-parkinsonian motor features: bradykinesia, resting tremor, rigidity, gait difficulty
vascular dementia: presentation
usually occurs after an infarct in a strategic location or with extensive white matter changes
does not cause visual hallucinations
CN I
Olfactory: smell
CN II
Optic: vision
CN III
Oculomotor: most EOMs, opening eyelids, pupillary constriction
CN IV
trochlear: down and inward eye movement
CN V
trigeminal: muscles of mastication; sensation of face, scalp, cornea, mucous membranes, nose
CN VI
abducens: lateral eye movement
CN VII
facial: move face, close mouth and eyes, taste (anterior 2/3), saliva and tear secretion
CN VIII
acoustic: hearing and equilibrium
CN IX
glossopharyngeal: phonation (1/3), gag reflex, carotid reflex swallowing, taste (posterior 1/3)
CN X
vagus: talking, swallowing, general sensation from the carotid body, carotid reflex
CN XI
spinal accessory: movement of the trapezius and sternomastoid muscles (shrug shoulders)
CN XII
hypoglossal: moves the tongue
CN III palsy
ptosis
dilated pupil
diplopia
eye deviated laterally and downward
Mini-mental status exam
ORArL 2, 3 RWD
Orientation to place AND time
Recognition (repeat three objects)
Attention (serial 7s counting backward from 100)
recall (ask to recall 3 objects 5 mins later)
Langauge
2 Identify names of 2 objects
3 Follow a 3-step command
Reading (e.g. Read this statement to yourself, do exactly what it says but do not say it aloud: “Close your eyes.”)
Writing
Drawing
Scoring:
- 0-17: severe dementia/delirium
- 18-23: mild dementia/delirium
- 24-30: no cognitive impairment
TIA classifications: vertebrobasilar
Occur as a result of inadequate blood flow from vertebral arteries
Presentations:
-vertigo
-ataxia
-dizziness
-visual field deficits
-weakness
-confusion
TIA classifications: carotid
due to carotid stenosis
Presentations:
-altered LOC
-aphasia, dysarthria
-weakness
-numbness
TIA: labs/Dx
CT: best for distinguishing between ischemia, hemorrhage, and tumor
MRI: best for detecting ischemic infarcts
EKG
Echocardiogram
Carotid doppler and ultrasound
Cerebral angiography
TIA: management
Aspirin
Plavix
Assess for HTN
CEA
- symptomatic low risk patients with 50-90% stenosis
- asymptomatic patients with >70% stenosis
CVA: labs/Dx
Large vessel stroke workup
-telemetry
-TEE with bubble study
-carotid imaging (US, CTA, MRA, angio)
-intracranial imaging (CTA, MRA, angio)
LP if grade I or II aneurysm to detect xanthochromia, but obtain head CT first
- contraindicated with large bleeds as brain stem herniation can be induced with rapid decompression of the subarachnoid space
CVA: Management by time of onset
<4.5 hours: tPA
- For thrombotic strokes, preferably <3 hours
<6 hours: mechanical embolectomy for all
6-24 hours: mechanical embolectomy for some
CVA: indications for ICP monitoring
Moderate: severe head injury who can’t be serially neurologically assessed
Severe head injury (GCS <8) + abnormal CT scan
Severe head injury (GCS <8) + normal CT if two of the following are present:
- Age >40
- BP <90
- Abnormal motor posturing
CVA: management for vasospasm
MAP goal 110-130 to treat cerebral vasospasm (if MCA spasms, it could interrupt blood flow to the brain and risk distal infarct)
Nimodipine (CCB) to counter vasospasm by preventing calcium from entering smooth muscle cells and causing contraction
Simple partial seizure
Common with cerebral lesions
No LOC
Rarely lasts >1 minute
Motor symptoms often start in single muscle group and spread to entire side of body
Parasthesias, flashing lights, vocalizations, hallucinations
Complex partial seizure
Common with cerebral lesions
Rarely lasts >1 minute
Motor symptoms often start in single muscle group and spread to entire side of body
Parasthesias, flashing lights, vocalizations, hallucinations
May have aura, staring, or automatisms such as lip smoking and picking at clothing
Followed by impaired level of consciousness
Absence (petit mal) seizure
Type of generalized seizure
Sudden arrest of motor activity with blank stare
Commonly discovered in children/adolescents
Begin and end suddenly
Tonic-clonic (grand mal) seizure
Type of generalized seizure
May have aura
Begins with tonic contraction (repetitive involuntary contraction of muscle), LOC, then clonic contractions (maintained involuntary contraction of muscle
Usually lasts 2-5 minutes
Incontinence may occur
Followed by postictal period
Status epilepticus
Seizure lasting >5 mins or more than 1 seizure within a 5-minute period without returning to normal level of consciousness
May occur when the patient is awake or asleep, but never regains consciousness between attacks
MEDICAL EMERGENCY
Seizures: assessment, labs/Dx
Assessment:
-presence of aura
-onset
-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: most important test in determining classification
CT: indicated for all new onset seizures to r/o brain tumor
Seizures: management: Stabilization Phase
0-5 minutes
Stabilize: ABC’s, disability? neuro exam
Time seizure from onset
Ongoing vital signs assessment
O2 per n/c or mask; consider intubation
Continuous EKG monitoring
FSBG: if <60, IV thiamine and 50ml dextrose
Routine labs, tox screen, anticonvulsant levels
Seizures: management: Initial Therapy Phase
5-20 minutes
Choose one of the following:
- IM midazolam
- IV lorazepam
- IV diazepam
If none of these are available, choose one:
- IV pheonobarbital
- rectal diazepam
- intranasal midazolam, buccal midazolam
Seizures: management: Second Therapy Phase
20-40 minutes
Choose one of the following:
- IV fosphenytoin
- IV valproic acid
- IV keppra
If none of these are available:
- IV phenobarbital if not previously given
Seizures: management: Third Therapy Phase
40-60 minutes
Repeat second-line therapy OR
Anesthetic doses: choose one (with continuous EEG monitoring)
- thiopental
- midazolam
- pentobarbital
- propofol
Subsequent seizure prevention
Maintenance doses of long-acting anticonvulsants
-valproic acid (Depakene)
-phenobarbital (Luminal)
-phenytoin (Dilantin)
-carbamazepine (Tegretol)
-ethosuximide (Zarontin)
-primidone (Mysoline)
Myasthenia Gravis: cause
Autoimmune disorder resulting in the reduction of the number of acetylcholine receptor sites at the neuromuscular junction
Variable clinical course with remissions and exacerbations.
Myasthenia Gravis: incidence
Mostly 20-40 years old but may occur at any age
Incidence peaks in the 30s for females, 50-60s for males
More common in women
Myasthenia Gravis: S/Sx
Ptosis (common 1st complaint)
Diplopia
Dysarthria
Dysphagia
Respiratory difficulty
Extremity weakness, typically worse after exercise and better after rest
Fatigue
Sensory modalities and DTRs are normal
Myasthenia Gravis: labs/Dx
Antibodies to acetylcholine receptors
Myasthenia Gravis: management
Neurology referral
Anticholinesterase drugs block the hydrolysis of acetylcholine
- used for symptomatic improvement
- pyridostigmine bromide (Prostigmin)
Immunosuppressives
Plasmapheresis
Ventilator support during a crisis if needed
Multiple Sclerosis: Cause
Autoimmune disease marked by numbness, weakness, loss of muscle coordination, and problems with vision, speech, and bladder control
The body’s immune system attacks myelin
Variable clinical course with remissions and exacerbations
Multiple Sclerosis: Incidence
Greatest incidence is in young adults ages 20-50
Multiple Sclerosis: S/Sx
Weakness, numbness, tingling, or unsteadiness in one limb; may progress to all limbs (common 1st complaint)
Spastic paraparesis
Diplopia
Disequilibrium
Urinary urgency or hesitancy
Optic atrophy
Nystagmus
Multiple Sclerosis: labs/Dx
MRI: most specific, shows damaged myelin sheath
Evoked potentials test
LP
Blood tests to rule out other causes
Multiple Sclerosis: management
No treatment to prevent progression
Neurology referral
Recovery from acute relapses hastened by steroids
Antispasmodics
Interferon therapy
Immunosuppressive therapy
Plasmapheresis
Guillain-Barré syndrome
Acute, usually rapidly progressive form of inflammatory polyneuropathy characterized by demyelination of peripheral nerves resulting in progressive symmetrical ascending paralysis
Guillain-Barré syndrome: cause
Usually preceded by a suspected viral infection accompanied by fever 1-2 weeks before onset of acute bilateral muscle weakness in lower extremities
Flaccid paralysis can result within 48-72 hours
Guillain-Barré syndrome: S/Sx
Typically, a rapidly progressive ascending paralysis
Cranial nerve impairment, as evidenced by difficulties in speech, swallowing, and mastication
Hypoactive/absent reflexes
Impairment of the muscles of respiration as paralysis ascends
Guillain-Barré syndrome: labs/Dx
CBC: early leukocytosis with left shift
LP
-CSF protein elevated, especially IgG
MRI
CT
Guillain-Barré syndrome: management
Supportive treatment while myelin is regenerated
Symptoms begin to recede within 2 weeks with recovery in 2 years
Neuro consult
Meningitis
infection of the membranes of the Pia mater and arachnoid mater of the brain or spinal cord
What should be considered in any patient with fever and neurologic symptoms, especially if there is a history of other infection or head trauma?
meningitis
Meningitis: pathogens
streptococcus pneumoniae
hemophilus influenzae
neisseria meningitidis
Meningitis: S/Sx
fever 38.3-39.4C (101-103F)
severe headache
N/V
nuchal rigidity
+Kernig’s sign
+Brudinski’s sign
photophobia
seizures
Kernig’s sign
pain and spasms of the hamstrings
Brudinski’s sign
Legs flex at both the hips and knees in response to flexion of the head and neck to the chest
Meningitis: labs/Dx
LP as soon as the diagnosis is suspected. CSF:
- cloudy or xanthochromic
- elevated pressure (bacterial)
- elevated protein
- decreased glucose
- +WBCs
Head CT
Meningitis: organism and management if <50
organism:
- N. meningitidis
- S. pneumoniae
vancomycin + ceftriaxone
Meningitis: organism and management if >50
Organism:
- S. pneumoniae
- N. meningitidis
- gram negative enterics (E. coli, Klebsiella, Enterobacter)
- L. monocytogenes
vancomycin + ampicillin + ceftriaxone
Cushing’s Triad
physiological nervous system response to acute elevations of intracranial pressure
Widening pulse pressure (SBP increases in an attempt to maintain a constant CPP)
Decreased RR
Decreased HR
Battle’s sign
bruising behind the ear at the mastoid process
sign of TBI
raccoon eyes
sign of basilar skull fracture
SCI to C4 or above: S/Sx
tetraplegia
may require mechanical ventilation
SCI to C4-C5: S/Sx
tetraplegia
control of head, neck, shoulders, trapezius, and elbow flexion
SCI to C5-C6: S/Sx
tetraplegia
some extension of wrist, index finger, thumb
SCI to C6-C7: S/Sx
elbow extension
capable of feeding, dressing
SCI to C7-T1: S/Sx
hand movement
SCI to T1-T2: S/Sx
paraplegia
upper extremity control but no trunk control
SCI to T3-T8: S/Sx
some trunk control
SCI to T9-T10: S/Sx
bowel and bladder reflex
moves trunk and upper thigh
SCI to T11-L1: S/Sx
Most leg and some foot movement
ambulation possible
SCI to L1-L2: S/Sx
lower legs, feet, perineum
bowel, bladder, sexual dysfunction if S2-S4 spinal nerves are involved
SCI: labs/Dx
spinal x-ray series
CT
MRI
SCI: management
Consult neurology/neurosurgery
Methylprednisolone 30mg/kg IV bolus, followed by an infusion of 5.4 mg/kg/hr for 23 hours
-indicated for blunt trauma but not penetrating trauma
SCI complications: C4 or above
respiratory compromise
SCI complications: T4-T6
may lead to autonomic dysreflexia
autonomic dysreflexia: S/Sx
diaphoresis and flushing above the level of injury
chills and severe vasoconstriction below the level of injury
hypertension
bradycardia
headache
nausea
autonomic dysreflexia: treatment
stimulus removal
antihypertensives
Brown Sequard Syndrome
Complication of SCI
Caused by damage to one half of the spinal cord
Brown Sequard Syndrome: S/Sx
IPSILATERAL upper motor neuron paralysis and loss of proprioception
CONTRALATERAL loss of pain and temperature
Brown Sequard Syndrome: treatment
MRI
steroids
Cauda Equina Syndrome
complication of SCI
Caused by compression of nerve roots at the end of the spinal cord (cauda equina)
Cauda Equina Syndrome: S/Sx
numbness in the lower legs, feet, or saddle region (groin, buttocks, genitals)
Cauda Equina Syndrome: management
MRI
steroids
surgery for decompression
Neurogenic shock
Complication of SCI to T6 or above
disruption of transmission of sympathetic impulses causing unopposed parasympathetic stimulation which leads to loss of vasomotor tone, including massive vasodilation
Results in hypovolemia, decreased venous return, and decreased cardiac output
Neurogenic shock: treatment
sympathomimetic vasopressors (dopamine, norepinephrine) to maintain blood pressure
Parkinson’s Disease
A degenerative disorder as a result of insufficient amounts of dopamine in the body
Parkinson’s Disease: S/Sx
tremor: slow, most conspicuous at rest, may be enhanced by stress
rigidity
bradykinesia
wooden facies (mask-like face)
impaired swallowing
May see drooling
decreased blinking
Myerson’s sign (repetitive tapping over the bridge of the nose produces a sustained blink response; glabellar reflex)
Parkinson’s Disease: labs/Dx
None
Dx of exclusion
Parkinson’s Disease: management
Carvidopa-Levodopa (Sinemet)
Dopamine agonists (mimic dopamine)
- pramipexole (Mirapex)
- ropinirole (Requip)
- rotigotine (Neupro)
MAO-B inhibitors (help prevent the breakdown of dopamine)
- selegiline (Eldepryl, Zelapar)
- rasagiline (Azilect)
- safinamide (Xadago)
Causes of delirium
Toxins
Alcohol/drug abuse
Trauma
Impactions in the elderly
Poor nutrition
Electrolyte imbalances
Anesthesia
Causes of dementia
Alzheimer’s Disease - most common
Atherosclerosis
Neurotransmitter deficits
Cortical atrophy
Ventricular dilation
Loss of brain cells
Possible viral causes
Dementia: labs/Dx
DEMENTIA to rule out other diseases
Drug reactions/interactions
Emotional disorders
Metabolic/endocrine disorders
Eye and ear disorders
Nutritional problems
Tumors
Infection
Arteriosclerosis
Labs:
- CBC
- BMP
- LFTs
- B12
- VDRL
CT to rule out tumors
Alzheimer’s Disease
Development of multiple cognitive defects characterized by both memory impairment (impaired ability to learn new information and recall previously learned information) and one or more of the following:
- aphasia
- 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 overall acetylcholine deficiency throughout the body
Alzheimer’s Disease: S/Sx
aphasia
apraxia
agnosia
inability to plan, organize, sequence, and make abstract difference
limb rigidity
flexion posture
disorientation
gait disturbances
impaired memory/judgment
Alzheimer’s Disease: management
Neurology consult
Cholinesterase inhibitors – increase the availability of acetylcholine
- donepezil (Aricept): all stages of Alzheimer’s
- galantamine (Razadyne): mild to moderate Alzheimer’s
- rivastigmine (Exelon): mild to moderate Alzheimer’s
NMDA antagonist
- memantine (Namenda): moderate to servere Alzheimer’s
Combination preparation
- memantine and donepezil (Namzaric): moderate to severe Alzheimer’s
Alcohol Use Disorder: screening test
CAGE
C: Have you ever felt the 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)
Myotonic muscular dystrophy
Most common adult form of muscular dystrophy
Often present with sustained involuntary contraction of a group of muscles
Stiffness and difficulty releasing their grip
Muscular dystrophy
Autosomal dominant disease that often manifests in late childhood with gait abnormalities due to weakness of the foot dorsiflexors
Progression to weakness of the intrinsic muscles of the hands and wrist extensors, atrophy of facial muscles, ptosis
Other tissues may also be affected: cardiac arrhythmias, early frontal balding, endocrinopaties, testicular atrophy
Causes / Risk factors associated with intracerebral hemorrhage
hypertension
septic emboli
brain tumor
vascular malformations
bleeding disorders
CNS infections
stimulants
Causes/ risk factors associated with subarachnoid hemorrhage
aneurysms
treatment for increased ICP
ICP is typically treated when it is over 20 mm Hg
If no obvious causes of increased ICP are present, analgesics (e.g. fentany) are used if the patient is having subclinical pain or agitation
The progression of transtentorial herniation will require..
mechanical ventilation, as it leads to respiratory arrest
Also leads to hypertension and bradycardia
transtentorial herniation: presentation
headache
altered LOC
dilation of one pupil
ptosis
Leads to respiratory arrest, bradycardia, hypertension
idiopathic intracranial hypertension: presentation
headache
visual changes and disturbances
idiopathic intracranial hypertension: risk factors
female of childbearing age
obesity
hypothyroidism
recent treatment with a tetracycline
Horner syndrome
rare condition classically presenting with partial ptosis, miosis, and facial anhidrosis (absence of sweating) or hyperhidrosis due to a disruption in the sympathetic nerve supply
Honer syndrome: labs/Dx
MRA head/neck to rule out carotid artery dissection
Horner syndrome: management
Neurosurgery if aneurysm related
Vascular surgery if carotid artery dissection or aneurysm related
Gold standard for identifying an intracranial lesion
MRI with contrast
central cord syndrome
spinal cord injury where messages are unable to be transmitted to or from the brain below the level of injury
- upper extremity weakness out of proportion to lower extremity weakness
anterior cerebral artery supplies which parts of the brain
medial portions of the frontal and parietal lobes and corpus callosum
part of the brain that is partially responsible for voluntary movement
frontal lobe
Visual loss is associated with an embolism in what part of the brain?
posterior cerebral artery
Aphasia is associated with an embolism in what part of the brain?
middle cerebral artery
Sensory loss is associated with an embolism in what part of the brain?
posterior cerebral artery
First step in treating delirium
rule out or remove reversible causes
When is intubation and ICP monitoring indicated?
Severe TBI w/GSC between 3-8 and abnormal head CT
normal pressure hydrocephalus: S/Sx
increasing urinary incontinence
cognitive decline with disinhibition and apathy
gait disturbance resulting in falls
Symptomatic cerebral salt wasting: treatment
3% NaCl
-rapidly increases serum sodium
Biggest concern with severe head injury
High priority: cerebral edema d/t increased intracranial volume, causing increased ICP and ultimately leads to cerebral tissues being oxygen-deprived
