Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
63 Cards in this Set
- Front
- Back
|
Transient global amnesia- dif dx
|
-TBI
-Seizure – temporal lobe -TIA -Migraine variant -Basilar artery thrombosis -PCA stroke |
|
|
Transient global amnesia- hx/cs
|
-Typically >50 yo
-Sudden onset memory loss of recent events and retention of new information -Preserved immediate recall and remote memory -Retention of self -Normal cognition otherwise -No longer than 24 hrs -Gradual memory return |
|
|
Transient global amnesia- dx tests
|
Labs: CBC, electrolytes, clotting tests
-EEG to r/o sz -CT/MRI to r/o structural abnormalities, stroke |
|
|
Transient global amnesia- tx/prognosis
|
-Resolves on its own w/ low recurrence rate
|
|
|
Transient global amnesia- pathophys
|
mediobasal temporal lobe and hippocampus (CA-1 area is most vulnerable to metabolic stress)
-Precipitating factors: physical exertion, overwhelming emotional stress, pain, cold water exposure, sexual intercourse, Valsalva maneuver = increased venous return to SVC |
|
|
Benign paroxysmal positional vertigo (BPPV)- dif dx
|
-Meniere’s disease
-Vestibular neuritis: lasts hrs to days -Chronic vestibulopathy -TIA -Orthostatic hypotension -Presyncope -Medication-induced dizziness -Phobic postural vertigo, psychogenic dizziness |
|
|
Benign paroxysmal positional vertigo (BPPV)- hx
|
-Vertigo occurs suddenly and unexpectedly triggered by sudden vertical head movements (looking up, bending down)
-Lasts 5-15 sec -Often hx of minor head trauma -Elderly -Absence of vomiting, tinnitus, hearing loss -May occur several times/day -Stops with repeated head movements |
|
|
Benign paroxysmal positional vertigo (BPPV) dx
|
-Dix-Hallpike maneuver: triggers vertigo episode with directional rotary nystagmus
|
|
|
Benign paroxysmal positional vertigo (BPPV) treatment
|
-Epley/canalith maneuver
|
|
|
Benign paroxysmal positional vertigo (BPPV) prognosis
|
-Usually spontaneously subsides over several wks to a few mos w/o tx
-Epley maneuver cures 57% |
|
|
Benign paroxysmal positional vertigo (BPPV) hx
|
Brief recurrent episodes of vertigo triggered by changes in head position that occurs 85% of the time with movement in the vertical plane
|
|
|
Epilepsy – simple partial seizure (focal)- dif dx (5)
|
-Syncope
-Migraine -Febrile sz -Benign childhood sz -Spell |
|
|
Epilepsy – simple partial seizure (focal)- history
|
-Consciousness is not impaired
-Sx limited to aura (if sensory in origin) or motor jerking (if motor in origin) -May secondarily generalize -May impair memory |
|
|
Epilepsy – simple partial seizure (focal)- cs
|
-Signs and sx may be motor (twitching of hand, arm, face, legs, trunk), sensory, autonomic
-May last secs to hrs -Todd paralysis |
|
|
Epilepsy – simple partial seizure (focal)- dx tests
|
-Determine seizure etiology
-Serum electrolyte and LFTs, CBC -MRI: to examine for small masses -Dx: unilateral EEG findings -Scalp EEG: -Interictal epileptic discharges (IEDs) are the clinical neurophysiologic hallmark of partial seizures w/ PDS as the cellular correlate of IED |
|
|
Epilepsy – simple partial seizure (focal)- treatment
|
-Valproate
-Oxycarbazepine - Phenytoin -Vagus nerve stimulator: adjunct treatment, activated at onset of seizure causes SZ to stop; increased efficacy over time |
|
|
Epilepsy – simple partial seizure (focal)- prog
|
-Adequate response to therapy
-After 1st seizure, risk of developing subsequent sz is 25-50% |
|
|
Todd paralysis is
|
transient hemiparesis of the side of the body involved in the seizure; resolves within hours
|
|
|
Epilepsy – simple partial seizure (focal)- pathophys
|
Focal seizures recur at the same location and should not move around
-Cause: may be idiopathic or d/t brain disease -Caused by increased excitation or impaired inhibition |
|
|
Epilepsy – simple partial seizure (focal)- pathophys initiation
|
Initiation:
-hypersynchronous discharges (paroxysmal depolarization shift – PDS) d/t hyperexcitable epileptic neurons w/in epileptic focus -causes sustained plateu-like depolarization (influx of Ca & Na) & burst of repeated APs followed by rapid repolarization & hyperpolarization |
|
|
Epilepsy – simple partial seizure (focal)- pathophys propigation
|
Propagation: seizure spreads when activation to recruit neurons surrounding epileptic focus 1) leads to a loss of surrounding inhibition and spreads to contiguous areas via local cortical connections and 2) spreads to distant areas by long association pathways
-Seizures are also propagates due to an increase in extracellular K+, which blunts the extent of hyperpolarizing outward K+ circuits depolarizesneighboring neurons -Accumulation of Ca in presynpatic terminals enhanced NT release -Depolarization-induced activation of NMDA receptors causes more Ca influx & neuronal activation |
|
|
Epilepsy – simple partial seizure (focal)- pathophys termination
|
-Termination: seizures stop spontaneously; Acid-sensing ion channel (ASIC1a) is sensitive to extracellular pH & regulates neuron excitability shortens SZ duration & prevents progression
|
|
|
Epilepsy – complex partial seizure (temporal lobe or psychomotor)- hx
|
-May begin with an aura (rising/falling sensation in abdomen, disgusting smell, or limb jerks) or without warning
-Consciousness is impaired, no recall |
|
|
Epilepsy – complex partial seizure (temporal lobe or psychomotor)- dif dx
|
-Mesial temporal lobe sclerosis
-Neoplasms -Cortical malformation -Stroke -Vascular malformation -Hypoxic-ischemic brain injury -CNS infection -Head trauma -Febrile sz -Absence sz |
|
|
Epilepsy – complex partial seizure (temporal lobe or psychomotor)- cs
|
-Pt may sit, walk, mumble, and often exhibit autonomic acts such as lip smacking and repetitive hand jesters
-Pt may wander aimlessly -Pt will not respond to visual or verbal stimuli -Lasts 1-3 min -Usually followed by a 5-20 min period of confusion -May be followed by tonic-clonic sz |
|
|
complex partial seizure (temporal lobe or psychomotor)- tx
|
-Mesial temporal sclerosis:
typically no response to anticonvulsant therapy; -Carbamazepine: inhibits voltage-dep Na channels; (SE- ataxia, dizziness, diplopia, blood dyscrasia) -Oxycarbazepine -Phenytoin anterior temporal lobectomy curative in 75% -Vagus nerve stimulator: adjunct treatment w/ uncertain mechanism |
|
|
Epilepsy – complex partial seizure (temporal lobe or psychomotor)- dx tests
|
-EEG: interictal spikes coming from temporal or frontal lobe
-T2 MRI: hyperintensity of hippocampus, eventually progresses to atrophy |
|
|
Epilepsy – complex partial seizure (temporal lobe or psychomotor)- prognosis
|
-Mortality rate among pts w/ epilepsy is 2-3 times that of the general pop
|
|
|
Epilepsy – complex partial seizure (temporal lobe or psychomotor)- pathophys
|
mesial temporal sclerosis: older children
progressive loss of neurons and gliosis in one hippocampus; may be d/t subtle brain damage (trauma, meningitis, hypoxia) from early childhood -Onset in 80% is temporal lobe; 20% in frontal lobe -30% of pts may have tumor, A/V malformation, hamartoma, etc in either temporal or frontal lobe -Most common form of seizure & most difficult to treat |
|
|
Epilepsy – primary and secondary generalized / tonic-clonic or grand mal- dif dx
|
-Complex partial sz
-Frontal lobe epilepsy -Migraine variant -Electrolyte imbalances -Nocturnal paroxysmal events -Syncope -Transient global amnesia -Psychogenic sz -Migraine variant |
|
|
Epilepsy – primary and secondary generalized / tonic-clonic or grand mal- hx
|
-LOC occurs w/o warning
-No recall of actual event -50% experience aura: sinking, rising, gripping, or unnatural sensation that may be accompanied by movements such as head and eye turning |
|
|
Epilepsy – primary and secondary generalized / tonic-clonic or grand mal- cs
|
-Marked increase in all muscle tone (tonic) for 2-30 sec followed by rhythmic (clonic) jerks w/ a gradual slowing or rate and abrupt stopping after 20-60 sec
-Pt is unconscious during sz and slowly recovers over min-1 hr -Tongue biting -Urinary incontinence |
|
|
Epilepsy – primary and secondary generalized / tonic-clonic or grand mal- dx test
|
-In an unprovoked 1st seizure, always order CT scan without contrast to rule out intracranial hemorrhage, tumor, infection, etc
-Dx: Bilateral EEG findings; fast spike-and-wave activity at 4-5 Hz |
|
|
Epilepsy – primary and secondary generalized / tonic-clonic or grand mal- tx
|
-Valproate
-Phenytoin: inhibits voltage Na channels; SE- nystagmus, ataxia, gum hyperplasia, hirsutism -Lamotrigine -Continue anticonvulsants for at least 2 yrs after last sz -If 3 meds fail, can consider vagal nerve stimulators or surgical removal of seizure focus |
|
|
Epilepsy – primary and secondary generalized / tonic-clonic or grand mal- prognosis
|
-2/3 of pts are well controlled on medications
-Complications can include: head trauma, tongue, lip, cheek trauma, aspiration pneumonia, cardiac arrhythmias, neurogenic pulm edema, sudden death |
|
|
Epilepsy – primary and secondary generalized / tonic-clonic or grand mal- pathophys
|
-Pathophys: paroxysmal high-frequency or synchronous low-frequency electrical discharge that can arise from almost any part of cerebral cortex
-Can be provoked by lack of sleep, excitation, alcohol -May be caused by a complex partial seizure w/ a warning (aura) -Aura: seizure began focally and secondarily generalized; represents the part of the brain that malfunctioned first and is a partial seizure |
|
|
Epilepsy – absence (generalized) / petit mal- dif dx
|
TIA
-ADHD -Psychogenic seizure -Breath holding spells |
|
|
Epilepsy – absence (generalized) / petit mal-hx
|
-Pts are age 3-20
-Precipitated by hyperventilation -No recall of event -School teachers often think child is daydreaming -Global arousal, postural control, & contents of ongoing memory are spared |
|
|
Epilepsy – absence (generalized) / petit mal-phys
|
-Rapid onset of speech arrest and unresponsiveness that lasts ~10 sec
-Often staring w/ eye blinking or lip movements -Increase or decrease in muscle tone -Minor body jerks -Immediate recovery -No loss of muscle tone |
|
|
Epilepsy – absence (generalized) / petit mal- dx test
|
-EEG: synchronous 3-Hz spike and wave discharges diffusely in both hemispheres
-EEG: spike slow wave spike slow wave… |
|
|
Epilepsy – absence (generalized) / petit mal- tx
|
-Ethosuximide: blocks voltage-dependent T Ca2+ channels; SE- headache, GI distress, ataxia, blood dyscrasia
-Valproate: inhibits voltage-dependent Na channels; side effects- GI distress, ataxia, wt gain, hepatic dysfunction |
|
|
Epilepsy – absence (generalized) / petit mal- prog
|
-In 2/3, spontaneously subside in adulthood
-May progress to primarily generalized sz or atypical absence sz |
|
|
Epilepsy – absence (generalized) / petit mal- pathophys
|
Brief seizures that do not cause loss of muscle tone
-Origin: deep diencephalic structures w/ early spread of seizure throughout both hemispheres -Epileptic neurons are highly prone to produce high frequency bursts of action potentials runaway excitation if system is not sufficiently controlled by inhibition |
|
|
Juvenile myoclonic epilepsy (JME)-dif dx
|
-Absence seizures
-Benign childhood epilepsy -Frontal lobe epilepsy -Tonic-clonic seizures -Myoclonus -Partial sz with secondary generalization |
|
|
Juvenile myoclonic epilepsy (JME)- hx
|
-Myoclonus occurring shortly after awakening
-Precipitants: stress, sleep deprivation -Onset in adolescence -17-49% have family hx of epilepsy |
|
|
Juvenile myoclonic epilepsy (JME)-physical
|
-Normal intelligence
-No LOC during jerks -GTCS in 80% of pts -Absence sz in 28% |
|
|
Juvenile myoclonic epilepsy (JME)- dx tests
|
-Sleep-deprived EEG w/ hyperventilation: generalized 4-6 Hz spike or polyspike and slow wave discharges lasting 1-20 sec
-CT/MRI: normal |
|
|
Juvenile myoclonic epilepsy (JME)- tx
|
-Lifelong anticonvulsants:
often valproate monotherapy , Keppra, Depakote (for multiple types of sz) -Seizure precautions: driving restrictions |
|
|
Juvenile myoclonic epilepsy (JME)- prog
|
-Responds well to treatments
|
|
|
Juvenile myoclonic epilepsy (JME)- Pathophys
|
idiopathic generalized epileptic syndrome of: myoclonic jerks, generalized tonic-clonic seizures (GTCSs), and sometimes absence seizures
-Occurs in late childhood to early adulthood -Tied to defects in calcium and chloride channel genes |
|
|
Meniere’s disease / Idiopathic endolymphatic hydrops -dif dx
|
-BPPV
-Vestibular migraine -Middle ear infection w/ inflammatory toxins -Inner ear trauma -Perilymphatic fistulas from cholesteatomas -Chronic vestibulopathy -Multiple sensory deficit syndrome -Presyncope |
|
|
Meniere’s disease / Idiopathic endolymphatic hydrops- hx/phys
|
-Spontaneous unprovoked attacks of vertigo associated w/ transient hearing loss, tinnitus, and aural fullness
-No trigger -Persists 1-several hrs -Abrupt onset of spinning -May have N/V -Typically unilateral -During attack, pts are often in distress, diaphoretic, pale |
|
|
Meniere’s disease / Idiopathic endolymphatic hydrops- dx tests
|
-Labs: rule out metabolic disturbances, infections, hormonal imbalances: TSH, glucose, ESR, ANA; CBC, electrolytes
-CT/MRI to r/o structural lesions -Audiometry tests -ECOG test |
|
|
Meniere’s disease / Idiopathic endolymphatic hydrops- tx
|
-Symptomatic control of nausea & vertigo via anticholinergics, antihistamines, promethazine IV or suppository, benzos, or phenothiazines
-Prednisone -Prevention (difficult): low NaCl diet, HCTZ, gentamycin in inner ear (can cause deafness), vestibular nerve section |
|
|
Meniere’s disease / Idiopathic endolymphatic hydrops- prog
|
-Over time, pt loses all frequencies of hearing and becomes deaf w/ all neurosensory elements in inner ear being destroyed
-Many pts are unable to work -Variable prognosis |
|
|
Meniere’s disease / Idiopathic endolymphatic hydrops- pathophys
|
Increased hydraulic pressure within the inner ear's endolymphatic system.
(1) fluctuating hearing loss (sometimes good or bad); (2) episodic vertigo (can be violent); (3) tinnitus or ringing in the ears (usually low-tone roaring); and (4) aural fullness (pressure, discomfort, fullness sensation in the ears) |
|
|
Meniere’s disease / Idiopathic endolymphatic hydrops- etiology
|
Unknown etiology, possible d/t rupture of endolymphatic membrane allowing rapid admixture of perilymphatic and endolymphatic fluid that produces electrolyte and ionic changes
|
|
|
Narcolepsy- dif dx
|
-Idiopathic hypersomnolence
-Sleep deprivat. -RLS -OSA -Depression -Circadian rhythm disorders -Sedating meds -Complex partial epilepsy -TBI -Malingering (drug-seeking) |
|
|
Narcolepsy- hx/phys
|
-Excessive daytime sleepiness
-Sleep attacks -Hypnagogic hallucinations: vivid hallucinations at sleep initiation or at awakening -Sleep paralysis: inability to move when falling asleep or awakening -Cataplexy: sudden loss of muscle tone triggered by strong emotions while maintaining consciousness -Obesity is common |
|
|
Narcolepsy- dx tests
|
-Rule out RLS, seizure
-EEC -ECG for syncope -Genetic testing -Nocturnal polysomnography followed by multiple sleep latency testing -CSF: hypocretin-1 < 110 pg/mL |
|
|
Narcolepsy- tx
|
-Modafinil, armodafinil
-Sodium oxybate -Selegiline -Adderall -Light meals -Nap scheduling -Counsel about driving restrictions |
|
|
Narcolepsy- prog
|
-Sleepiness diminishes with age
-Cataplexy may resolve with or without tx |
|
|
Narcolepsy- pathophys
|
Recurrent irresistible attacks of daytime sleepiness, often in conjunction with triad of cataplexy, sleep paralysis, and hypnagogic hallucinations
-Related to reduced hypocretin/orexin levels in hypothalamus, pons, cortex -Often have positive family hx |
