Neuro 2 Flashcards
Criteria for epilepsy diagnosis
- two or more unprovoked seizures occur
- one seizure occurs in a person whose risk of occurrence is at least 60%
- one or more seizures occur in context of known epilepsy syndrome
Top five RF for seizure disorder?
head trauma, stroke, infectious disorders, toxic-metabolic disorders, drug and alcohol withdrawal
Primary neurologic disorders related to seizures:
benign febrile convulsions of childhood, idiopathic/cryptogenic seizures, cerebral dysgenesis, symptomatic epilepsy
Treatment of eclampsia
magnesium sulfate
What is porphyria?
disorder of heme synthesis, produces neuropathies and seizures
Treatment of porphyria
gabapentin, pregabalin, levetiracetam
Drug toxicity and drug withdrawal typically results in what type of seizure?
generalized tonic-clonic
Unusual drug that causes seizures?
isonazid
When does EtOH withdrawal occur?
within 48 hours of cessation and resolves within 12 hours
When does sedative withdrawal occur?
within 2-4 days, but can be delayed to 1 week
At what age do benign febrile convulsions occur?
6 months to 5 years
When do benign febrile convulsions occur?
first day of a febrile illness (temp >100.4)
How long do seizures of benign febrile convulsions occur?
10-15 minutes and lack focal features
Treatment for benign febrile convulsions?
usually self-limited; can treat with diazepam or buccal midazolam; for recurrences–intermittent oral diazepam at onset of febrile illness
Idiopathic seizures account for x of all new -onset seizures
2/3
Seizures within x week after non-penetrating injury are not predictive of a chronic seizure disorder
first week
seizures are more commonly seen with hemorrhagic or ischemic stroke?
hemorrhagic
Non-epileptic seizures are generally what type?
general tonic-clonic with warning
What differentiates non-epileptic seizures?
No LOC, no postictal confusion, EEG does not show organized seizure activity
If a seizure/spell event occurs with flaccid unresponsiveness what is likely?
hypoperfusion
If flaccid unresponsiveness due to hypoperfusion is prolonged it can lead to brief stiffening or jerking, called:
convulsive syncope
Post-ictal state follows what type of seizure?
generalized tonic-clonic
A prolonged postictal state follows what type of seizure?
status epilepticus
Tongue biting is indicative of what type of seizure?
gernalized tonic-clonic
Three essential elements of seizure diagnosis?
clinical presentation; specific triggers or provoking event; detailed description of event
Herpes simplex encephalitis EEG
hi volt 3/sec TL
CJD EEG
burst suppression
hepatic encephalopathy EEG
bilateral synchronous triphasic waves
Four key principles of seizure management
1) establish the diagnosis of epilepsy before starting drug therapy
2) choose the right drug for seizure type
3) treat the seizures rather than the serum drug level
4) evaluate one drug at a time
Two MOI of anticonvulsants
- potentiating inhibitory GABA synaptic transmission
- inhibiting excitatory (glutamatergic) transmissions
Nearly all seizure meds can have the SE of?
blood dyscrasias and hepatic toxicity
SE of Lamotrigine
SJS in first 8 weeks
Phenytoin treats:
PGS
Valproic acid treats:
PGSMA
Levetiracetam treats:
PGM
Lamotrigine treats:
PGSA
A seizure can be considered refractory after treatment for?
2 years
Epilepsy itself is associated with what birth defects?
still birth, microcephaly, seizure disorders
what two seizure drugs are associated with neural tube defects?
valproic acid and carbamazepine
What’s the safest anticonvulsant in pregnancy?
Lamotrigine
All women on anticonvulsant drugs of child bearing age are given?
1 mg/day of folate
What types of seizures are at little risk to a fetus?
partial and absence seizures
Which drug needs to be monitored closely due to levels needing to be doubled or tripled during pregnancy?
Lamotrigine
When should you consider withdrawing a patient’s seizure meds?
After 2-5 years of being seizure free
When removing a seizure med how long should you taper?
6 weeks minimum
Which form of seizure (broadly) has aura?
focal
Describe a simple partial seizure:
movements of single muscle group in face, limb, or elsewhere
In a simple partial seizure, if it spreads to involve neighboring regions of cortex it’s called?
Jacksonian march
Autonomic symptoms of a simple partial seizure?
pallor, flushing, sweating, piloerection, pupil dilation, vomiting, hypersalivation
Psychiatric symptoms of a simple partial seizure?
memory distortions, thought or cognitive deficits, affective disturbances, hallucinations or illusions
Is there LOC with simple partial seizure?
No
Is there postictal state with simple partial seizure?
yes
How long does postictal state last with simple partial seizures?
30 minutes to 36 hours
Complex partial seizure usually occurs in which lobe?
temporal lobe or medial frontal lobe
Is there LOC with complex partial seizure?
yes
Is there aura with complex partial seizure?
Yes (epigastric sensations, fear, deja vus, olfactory hallucinations)
Which form of aura is most common in complex partial seizures?
epigastric sensations
How long do seizures last in a complex partial seizure?
1-3 minuts
What does the EEG show in complex partial seizure?
shows focal TL spikes or appear normal
Partial seizures with secondary generalization look like what other type of seizure?
generalized tonic-clonic seizure
Partial seizures with secondary generalization are more likely in adults or children?
adults
Describe pathology of generalized seizures
depolarization during tonic phase, followed by rhythmic depolarization and repolarization during clonic phase
Do tonic clonic seizures have LOC?
yes
Do tonic clonic seizures have aura?
usually no
Sequence of a tonic clonic seizure?
tonic phase, clonic phase, recovery
What happens in the tonic phase of a tonic clonic seizure?
LOC, tonic contraction of limbs for 10-30 seconds; contraction or respiratory and masticatory muscles; patient falls to ground
What happens in the clonic phase of a tonic clonic seizure?
alternating muscle contractions and relaxation that is symmetric for 30-60 seconds; muscles then become flaccid; breathing returns; mouth may have frothing saliva; urinary incontinence
What happens in the recovery phase of a tonic clonic seizure?
confusion and HA; full orientation 10-30 minutes; PE normal, may have + Babinski sign; pupils alway sreact to light
Does tonic clonic seizures have a post-ictal state?
yes, usually a few minutes
Whats the big SE of valproic acid?
liver damage in children under ten
Is there LOC in absence?
yes, 5-10 seconds
Describe absence?
abrupt but brief LOC without loss of postural tone; may have subtle motor manifestations, eye blinking, staring, slight head turning; fully oriented after it stops
Three types of absence?
typical; atypical; with myoclonus
Describe a typical absence seizure?
abrupt cessation of activities, motionless, blank stare and loss of awareness lasting about 10 seconds; attack ends suddenly and resumes normal activities immediately
Describe an atypical absence seizure?
longer duration than typical, often accompanied by myoclonic, tonic, atonic, and autonomic features as well as automatisms
Describe an absence seizure with myoclonus:
absence with myoclonic components
When do absence seizures begin?
Always begin in childhood and rarely persist into adolescence or adulthood
Describe a tonic seizure?
sustained increase in muscle contraction lasting a few seconds to minutes; drop attacks; respiratory arrest and cyanosis; LOC
Describe a clonic seizure?
prolonged regularly repetitive contractions involving the same muscle group at a rate of 2-3 cycles per second; LOC
Describe a myoclonic seizure?
sudden, brief, shock-like, involuntary, single, or multiple contractions of muscle groups of various locations
What type of myoclonic seizures are most common?
juvenile myoclonic epilepsy
Two types of myoclonic seizure?
myoclonic atonic; myoclonic tonic
Describe atonic seizure?
sudden loss or diminution of muscle tone lasting 1-2 seconds, involving head, trunk, jaw, or limb musculature; loss of postural tone, leading to a fall or drop attack
Atonic seizures are most commonly seen in?
lennox-gastuat syndrome
How long does status epilepticus last?
5-30 minutes without ceasing OR seizures recur so frequently that full consciousness is not restored between episodes
What’s the word for excessive lymphocytes, indicating leukocytosis found in 15% of status epilepticus patients?
Postictal pleoyctosis
Drug therapy for status epilepticus control?
diazepam or lorazepam/midazolam initially; then phenytoin, repeat, phenobarbital. If ineffective use propofol.
Special health issues that may result from status epilepticus?
hyperthermia, lactic acidosis, leukocytosis
Describe confused?
disoriented; impaired thinking and responses
Describe delirious?
disoriented; restlessness, hallucinations, delusions
Describe drowsy or somnolent?
Can be aroused by minimal stimulus, but poor attention and easily falls back to sleep
Describe lethargic?
severe drowsiness in which the patient can be aroused by moderate stimuli and then drift back to sleep
Describe obtunded?
like lethargy in which the patient has a lessened interest in the environment, slowed responses to stimulation, and tends to sleep more than normal with drowsiness in between sleep states
Describe stuporous?
sleep like state (not unconscious); little/no spontaneous activity. Only vigorous and repeated stimuli will arouse the individual, and when left undisturbed, the patient will immediately lapse back to unresponsive state
Name the levels of consciousness:
conscious, confused, delirious, drowsy or somnolent, lethargic, obtunded, stuporous, comatose
The ladder of consciousness:
normal state –> vegetative state –> general anesthetic –> coma –> brain death
Coma results from?
lesions that affect the RAS or both hemispheres
Three things tested in Glasgow coma scale?
eye opening; best motor response; best verbal response
Scores for glasgow coma scale go from?
3-15
Is a high or low glasgow coma scale good?
high
coma glasgow scale?
3-8
a sudden coma is likely due to?
vasculary, especially brainstem stroke or SAH
rapid progression stroke is likely due to?
intracerebral
longer progression stroke is likely due to?
tumor, abscess, or chronic SDH
if stroke is preceded by confusion or agitation it’s likely due to?
metabolic or infectious cause
When does hypothermia occur in coma?
caused by ethanol or sedative drug intoxication, hypoglycemia, Wrnicke encephalopathy, hepatic encephalopathy, and myxedema
Coma with hyperthermia occurs when?
heat stroke, status epilepticus, malignant hyperthermia (related to inhalational anesthetics, anticholinergic drug intoxication, pontine hemorrhage, and certain hypothalamic lesions)
What type of eye condition strongly suggest subarachnoid hemorrhage?
subhyaloid hemorrhages (superficial retina)
Three signs of basilar skull fracture?
raccoon eyes, battle sign (swelling overlying mastoid bone), hemotympanum
How can CSF rhinorrhea and otorrhea be distinguished from nasal mucous?
beta-2 transferrin is unique to CSF
What size are the pupils in an opioid OD?
1-1.5 mm
Normal: 3-4 mm, equal, brisk and symmetric
metabolic or toxic cause
Thalamic: 2 mm reactive, early compression
mass lesions or swelling; interruption of descending sympathetic pathways
Fixed, dilated: >7 mm
usually compression of CN III and sympathetic nerve fibers; anticholinergic or sympathomimetic drug intoxication
Fixed, midsize: 5 mm
brainstem damage at the midbrain level, which interrupts both sympathetic, pupillodilator and parasympathetic, pupilloconstrictor nerve fibers
Pinpoint: 1-1.5 mm
focal pons lesion, or cerebellar (OCR absent); thalamic hemorrhage; opioid OD (OCR intact), organophosphate poisoning, miotic eye drops, neurosyphilis (Argyll Robertson pupils)
Anisocoria can indicate what type of lesion?
midbrain, CN, or eye lesion
Anisocoria of what difference is significant?
> 1 mm
Disconjugate deviation of eyes indicate?
structural brain stem lesion
Conjugate lateral deviation of eyes indicates?
ipsilateral poutine infarction OR contralateral frontal hemispheric infarction
Unilateral dilated, fixed pupil without consensual responses indicate?
supratentorial mass lesion, impending brain herniation, posterior communicating aneurysm
OCV in conscious patients?
nystagmus directed away from stimulus
OCV in comatose with intact brainstem?
Deviation of eyes toward stimulus; may see conjugate horizontal movements
Deviation of eyes toward stimulus; may see conjugate horizontal movements rules out?
brainstem lesion
Deviation of eyes toward stimulus; may see conjugate horizontal movements suggests?
metabolic or bilateral hemisphere lesion causes
OCV absent response seen in?
sedative drug intoxication, lesion in cerebellum or brainstem, peripheral vestibular disease
OCV downward deviation suggests?
drug intoxication
What OCV is seen in lesion of CN III?
ipsilateral eye abducts normally, but no adduction of contralateral eye
Decorticate:
elbow flex, shoulder adduction, leg ext/IR
Decorticate seen in?
thalamus or large hemispheric mass/effect compressing thalamus from above
Decerebrate:
elbow extension, shoulder/forearm IR, leg extension
Decerebrate seen in?
midbrain dysfunction, more severe damage usually
Benzodiazepine antagonist?
Flumazenil
Considered permanent vegetative state if x if non-traumatic
> 3 months
Considered permanent vegetative state if x if traumatic?
> 1 year
What four things can a coma lead to?
locked-in syndrome; vegetative state; chronic coma; brain death
Vegetative state can lead to what three things?
minimally conscious state to evolving independence; permanent vegetative state
Causes of locked-in syndrome?
pontine infarction, hemorrhage, central pontine myelinolysis, tumor, or encephalitis
How can you distinguish a vegetative state from a coma?
exhibit spontaneous eye opening and sleep-wake cycles
Vegetative state: absence of–
awareness of self or environment; purposeful or voluntary behavioral response to all stimuli; language comprehension or expression
Vegetative state: presence of:
intermittent wakefulness manifested by the presence of sleep-wake cycles; autonomic functions; cranial nerve and spinal reflexes
Vegetative state EEG
diffuse slow-wave activity; if severe, isoelectric EEG
Three conditions of diagnosis of brain death
preconditions showing irreversibility; signs showing complete cessation of all clinical brain functions; confirmatory tests
preconditions showing irreversibility for brain death
presence of a structural brain lesion sufficient to produce all clinical signs; absence of reversible significant toxic or metabolic encephalopathy; sequential repeated testing or one test followed by a confirmatory blood flow test
signs showing complete cessation of all clinical brain functions
coma; apnea; brainstem areflexia
What’s the most common disabling neurological disorder?
Stroke
Stroke is a syndrome characterized by these four key features:
sudden onset; focal involvement of the CNS; lack of rapid resolution; vascular cause
How long does a stroke have to occur to distinguish it from a TIA?
24 hours
Loss of consciousness occurs in less than x seconds after blood flow to brain has stopped
15 seconds
Irreparable damage to the brain tissue occurs within x of ischemia
5 minutes
Clinical symptoms of cerebral ischemia occur when global or regional blood supply falls below? #
50 mL per 100 g per minute
Global Ischemic Injury
occurs in the setting of complete cardiovascular collapse
Diffuse hypoxic injury
causes include travel to high altitude, severe anemia, pulmoary disease
focal ischemia
caused by occlusion of vessel
Cerebral hemorrhage
SAH, ICH
Cerebral edema
swelling
Five types of cerebral ischemia?
global ischemic injury, diffuse hypoxic injury, focal ischemia, cerebral hemorrhage, cerebral edema
Cerebral edema usually peaks between x and x after onset of ischemic injury?
48-72 hours
Which is more common hemorrhagic or ischemic strokes?
Ischemic
Ischemic death of brain tissue occurs when flow is less than? %
20% of normal
Damage to anterior cerebral artery
contralateral leg weakness
Middle cerebral artery injury
contralateral face and arm weakness greater than leg weakness, sensory loss, visual field cut, aphasia or neglect (depending on side)
Posterior cerebral artery injury
contralateral visual field cut
deep/lacunar injury
contralateral motor or sensory deficit without cortical signs (i.e. aphasia/apraxia/neglect/loss of higher cognitive functions), clumsy hand-dysarthria syndrome and ataxic hemiparesis
basilar artery injury
oculomotor deficits and/or ataxia with crossed sensory/ motor deficits
vertebral artery injury
lower cranial nerve deficits (vertigo/nystagmus/dysphagia or dysarthria and tongue/ palate deviation) and/or ataxia with crossed sensory deficits
Name some anti-coagulants
Warfarin, heparin
Name some anti-platelets
aspirin, clopidogrel
Name a thrombolytic
rtPA
IV administration of rtPA within x hours of onset
4.5 hours
Treatment of stroke should occur within x minutes of the patient’s arrival
60 minutes
Indications for rtPA
time of symptom onset <4.5 hours; measurable neurologic deficit; 4-22 on stroke scale; high risk patients often have early CT scan changes showing large area of edema or mass effect
Within the first 24 hours of administration of rtPA what shouldn’t be administered?
anticoagulants and antiplatelets
What should be avoided after rtPA
arterial puncture, placement of central venous lines, bladder cath, ng tubes
Stroke BP goal
<180/105 x 24 hours
What orally can occur after stroke?
orolingual angioedema
How does rtPA work?
binds to plasminogen and breaks down fibring strands in the blood clot
AE of rtPA?
fever, bleeding
advantage of rtPA
does not cause allergic reactions, does not induce hypotension
Other treatments for strokes?
intra-arterial thrombolysis; mechanical thrombectomy; carotid endarterectomy; carotid artery stenting; posterior fossa decompression; decompressive craniotomy
intra-arterial thrombolysis
intra-arterial administration of rtPA; 4.5-6 hours or with history of major surgery
Mechanical thrombectomy:
within 6 hours; clot retrieval
Carotid endarterectomy
surgical removal of thrombus from a stenotic common or internal carotid artery in the neck; indicated for patients with anterior circulation TIAs and high grade extracranial internal carotid artery stenosis
Carotid artery stenting AE
associated with an increased periprocedural stroke, but decreased periprocedural MI
Posterior fossa decompression for?
brainstem compression after cerebellar infarction
Decompressive craniectomy to prevent?
transtentorial herniation and death in patients younger than 60 years old who deteriorate within 48 hours after large hemispheric strokes
Secondary stroke prevention: BP goal
<140/85
Secondary stroke prevention: diabetes
<126
secondary stroke prevention: cholesterol
<200
secondary stroke prevention: LDL
<100
secondary stroke prevention: INR
2-3
