596193
Descripción
Fichas por Danielle Morley, actualizado hace más de 1 año
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Creado por Danielle Morley
hace más de 10 años
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| Pregunta | Respuesta |
| At what age does the posterior dominant rhythm begin to appear? What frequency is it seen to be at this time? | Begins to be seen at age 3 months at approx. 3Hz. |
| At what age should the posterior dominant rhythm reach 8Hz? | 3yrs |
| What is the normal frequency for the posterior dominant rhythm in adults? | 9-12Hz |
| Can a posterior dominant rhythm of less than 8Hz or less be considered normal? If so, in which circumstances? | Yes- normal in infants and children, elderly (80+). Normal in any age in drowsiness. |
| Can an asymmetrical posterior dominant rhythm be considered normal? If so, explain. Also what montage should be used to determine amplitude asymmetries? | Yes- handedness rule states that the posterior dominant rhythm may be up to 50% greater amplitude on the dominant side. However, most people, regardless of handedness, have PDR of greater amplitude on the right, so asymms of up to 35% lower on the right side are considered WNL. Amplitudes should be checked using a referential montage. |
| Can alpha be abnormal? If so, when? | Yes- ALPHA COMA!!, if asymm (>50% lower on non-dominant side or >35% lower on right) or unilateral, if slow for age/state, if intermixed epileptiform |
| Can it be normal for alpha to not be reactive to eye opening? Explain. | Yes- if patient is drowsy and/or eyes have been open for a period of time. Called "paradoxical alpha" |
| When is the best time to review the frequency of the posterior dominant rhythm? Why is this? | When patient is awake and alert and eyes have been closed for >2 seconds. Reason for waiting is "alpha squeak"- alpha rhythm is seen to be 1-2Hz faster in the 1-2secs immediately after eye closure. By waiting you get an accurate frequency. |
| At what age do sleep spindles begin to appear? Describe what they look like at this point. | Begin to appear age 48wks (2 months post term). Seen in bicentrals @ approx 14Hz, overall symmetrical, but asynchronous. Usually seen in trains of a few seconds (3-7sec), morphology is arciform. |
| By what age should sleep spindles be symmetrical? By what age should they be fully synchronous? | Should be generally symmetrical at all ages. Should become synchronous within the 2nd year of life. |
| In a 1yr old patient, sleep spindles are seen only on the right side. Is this normal or abnormal? Why or why not? | Abnormal. Sleep spindles can still be asynchronous at this age, but they should still be present generally the same amount bilaterally. |
| In what state(s) are spindles seen? | Stage 2 sleep, minimally in slow wave sleep (stages 3-4). Also seen in spindle coma. |
| Name the following pattern. What prognosis does this pattern hold? -Diffuse, non reactive, anterior max alpha | Alpha coma. Very poor prognosis. |
| Name the following pattern. What prognosis does this pattern hold? -Prominent, non-reactive, continuous spindle-like activity. | Spindle coma. Relatively good prognosis if reflexes are intact. If reflexes absent, poor prognosis. |
| Name indications of drowsiness on the EEG. | Waxing and waning or dropout of the posterior dominant rhythm. Slowing of the background/ appearance of theta. Appearance of rudimentary vertex waves and POSTS as approaching light sleep. Slow lateral eye movements and decreased muscle tone. |
| What does POSTS stand for? What does this pattern indicate? At what age is it seen? | Positive Occipital Sharp Transients of Sleep. Indicates stage 1-2 sleep. First seen in childhood but poorly defined. Seen max in adolescents and adults. |
| What is a pattern that is similar to POSTS? Under which conditions is this pattern seen? Is this normal or abnormal? | Lambda- seen commonly in children, less commonly in adults. Seen when awake/alert with eyes open and scanning. This is considered to be a normal variant. |
| What are some normal variants that mimic epileptiform activity? | Small sharp spikes (aka BETS- benign epileptiform transients of sleep), wicket spikes, 6Hz SW (phantom SW), SREDA (subclinical rhythmic EEG discharges in adults), RMTD (psychomotor variant), hypnagogic hypersynchrony |
| Name the following pattern. What condition(s) may this pattern be associated with? What prognosis does this pattern hold? -generalized sharp or tripasic discharges that are seen periodically @1-2 times per second | GPEDs- generalized periodic epileptiform discharges. Seen with classic CJD, severe anoxia. Could also be seen with severe toxic/metabolic condition, status epilepticus. Very poor with CJD, severe anoxia. Better prognosis with status epilepticus and toxic/metabolic conditions as these conditions are potentially resversible with treatment. |
| Name the following pattern. What condition(s) may be associated with this pattern. What prognosis does this pattern hold? -very high amplitude polyphasic mixed sharp and complexes. Complexes are stereotyped and periodic, occuring every 8 seconds. Myoclonic jerks are associated with the bursts. Underlying background is of normal amplitude, moderately abnormal. | SSPE discharges, seen with SSPE (subacute sclerosing panencephalitis). Poor prognosis (mortality high, those that survive often in vegetative/ severe MR state) |
| Give definition and clinical description of syncope. Also include common causes or triggers. | Syncope: transient loss off consciousness caused by cerebral hypoperfusion. Often preceded by presyncope- symptoms such as lightheadedness, loss of vision/blackout or tunnel vision, loss of hearing, sweating, feeling of heat, nausea/ abdominal discomfort, palpitations. LOC is brief (usually 5-30 seconds). The person comes around quickly and is not confused or disoriented. Tongue biting or incontinence is possible but uncommon. Usually occurs from standing position. Common causes are orthostatic hypotension, hypoglycemia, triggers such as sight of blood, pain, cardiac arrhythmias, etc. Commonly happens in the shower, in a hot room, at church, etc. |
| What EEG changes (if any) are seen during and after presyncope and syncope? | Presyncope: if presyncope occurs may show appearance of theta and/or delta slowing. Syncope: appearance of theta and/or delta slowing followed by high amplitude gen'd delta. If due to cardio-inhibitory causes, cerebral hypoperfusion tends to last longer (~40sec), and there will eventually be a sudden flattening of the background amplitude. Afterwards, background gradually returns to normal amplitude and frequency. **No epileptiform activity is seen.** |
| What is convulsive syncope? What causes it? What will an EEG during convulsive syncope show? How can it be differentiated form true seizure activity (ie GTC)? | Variant of syncope in which there are tonic or myoclonic movements. Convulsions/ involuntary movement are caused by the brain in response to hypoxia... Movements can range from a single twitch of the mouth to violent jerks affecting the entire body to head or body extension with either extension or flexion of the arms. EEG would show theta-delta slowing, then suppression of the background- convulsions would start at the suppression, ABSENCE of epileptiform activity. The main differentiating factors from a GTC would be: myoclonus is generally brief, arrhythmic, and multifocal (vs rhythmic sustained gen'd jerking), specific provocation for the event, and rapid reorientation. |
| Give a clinical description of migraine. What causes migraines? | Recurrent headaches (usually moderate to severe) that last 2-72hrs that are usually pulsatile in nature, affecting one side of the head, commonly associated with symptoms of nausea +/- vomiting, photo- and phono- phobia, generally made worse with activity. They may have up to 4 phases- PRODROME (alteration of mood, cravings, stiff muscles, etc 2hrs-2days before migraine pain), AURA (focal neuro signs during or before migraine- most commonly visual, sensory, or language disturbances), PAIN (sx noted above, uni- > bi- lateral), PAIN/HEADACHE (winding down of migraine, often dull ache or impaired thinking, hangover-like feeling for up to days after the migraine). CAUSE is thought to be neurovascular, with a genetic link. |
| What EEG changes (if any) are seen with migraines? | EEG is commonly normal. That said, during visual aura there may be some theta slow waves or depression of background amplitude. The most definitively abnormal EEGs occur during complex migraines such as hemiplegic migraine or migraine with disturbed consciousness- these may show unilateral or bilateral delta. |
| What is Moyamoya disease? Where did it get it's name? What population has the highest incidence of the disorder? Why it relevant to EEG? | Progressive ascular disorder characterized by narrowing/ constriction of the internal carotid arteries. Many tiny vessels may form to compensate for this. "Moyamoya" is Japanese for "puff of smoke" which is the characteristic appearance of the brain vessels as seen with angiography. Highest incidence is in those of Japanese descent. Affects children>adults. Is important for EEG as people with Moyamoya are susceptible to stroke, TIA, intracerebral hemorrhage, and THIS DISORDER IS A CONTRA-INDICATION TO HV. |
| What is Alzheimer's disease? What are the classic symptoms? What is the typical age of onset? What is the prognosis? What are the pathological findings/ causes? | Most common form of dementia. Classic symptoms are depression, memory, personality changes, social withdrawal, intellectual impairment, agitation, confusion/disorientation, wandering, poor self-care. Typical onset is age 65+ (senile), can also be btwn 30-60 (pre-senile). Prognosis- death usually within 6-8yrs from diagnosis (2-20yrs), more rapid w/ early onset. Causes: accumulation of beta-amyloid protein in brain leads to nerve cell death, some genetic factors; hallmark findings: deep cortical atrophy esp F-P, neurofibrillary tangles esp T-P, senile plaques/ amyloid plaques (=protein deposits) in association areas. |
| What are the EEG findings in Alzheimer's disease? | Gen'd findings. Waking- slowing/disturbance of PDR, increase of diffuse slow (EEG= predominantly theta), +/- F-T max diffuse intermittent delta. Sleep- disorganized, poorly formed or non-existent sleep potentials. In general- consistently abn, epileptiform rare, good correlation btwn level of cognitive impairment and degree of EEG abn. |
| What is Parkinson's disease? What are the classic symptoms? What is the typical age of onset? What is the prognosis? What are the pathological findings/ causes? What does typical treatment consist of? | Relatively common progressive unstoppable disorder of the CNS that is characterized by symptoms of bradykinesia (slowing of the initiation of movement), constant muscular rigidity, postural and gait abnormality, resting tremor (in 90%). Other secondary symptoms include depression, speech disturb, dementia, breathing/swallowing issues. Can appear at any age but usually >30yrs, increasing risk with age. Prognosis is generally good- quality of life tends to be negatively affected, life expectancy normal or slightly shortened. Thought to result from combination of genetic predisposition and (not yet identified) environmental factors. Caused by deterioration of neurons in substantia nigra (lewy bodies) of the basal ganglia- when normal, these produce dopamine (neurotransmitter). Treatment consists of replacing the dopamine (drug called levadopa)- helps symptoms but does not stop the progression of the disease. |
| What are the EEG findings in Parkinson's disease? | 2/3 normal. 1/3 mild diffuse slowing (more so than normal elderly), PDR less than 8Hz- level of EEG abn seems to correlated to level of cognitive and motor disability. |
| What is Lewy Body disease? What are the pathological findings/ causes? What are the symptoms? What age group does it usually affect? What is the prognosis? | Form of dementia caused by Lewy bodies (spherical deposits of abn neurofilament proteins and associated enzymes- similar to those in Parkinson's). Affects the elderly most- may represent 20% of cases of dementia in patients 70-80yrs old. Wide range of progressive symptoms depending on where the Lewy bodies occur- changes in alertness/attention, hallucinations, movement/posture issues similar to those in Parkinson's disease, confusion, memory loss (short and long term), muscle stiffness. Prognosis- survival is similar to Alheimer's disease- avg 8yrs after symptoms appear. |
| What are the EEG findings in Lewy Body disease? | Loss of PDR. Slow wave transients in temporal regions (50%). |
| What is Picks disease? What are the pathological findings? What is the typical age of onset? How does someone get this disease? What is the prognosis? What are the classic symptoms? | Rare progressive dementia. Tends to onset in mid-life (50-60yrs) caused by pale swollen neurons (called pick's antibodies) found in the brain (similar to the tangles of Alz), max F-T causing cell death and subsequent severe F-T atrophy. In rare variant, there is gen'd atrophy involving subcortical structures (caudate nucleus)- more common in younger patients. Acquired sporadically in 90%, familial (autosomal dominant) in the remaining 10%. Symptoms gradually appear in order: personality changes, disinhibition, *"child-like" behaviour, +/- aggressiveness/ compulsiveness *speech impairment, flat affect, mutism, memory and comprehension problems, mutism, eating and swallowing problems |
| What are the findings in Pick's disease? | Usually normal, PRESERVED alpha rhythm. |
| What is meningitis? Where does it come from/what causes it? What are the key symptoms? What are some other symptoms? What kind of outcome/prognosis is expected with meningitis? What factors affect prognosis and how so? What are some common long term issues that arise as a result of meningitis? | Inflammation of the meninges. Infection (bacterial, viral, fungal, etc) travels via bloodstream, CSF, cranial or spinal nerves, etc to infect the meninges. May also occur from seepage of infection though skull fracture; in infants may be acquired in utero via contaminated amnio. Key symptoms: fever, stiff neck, headache. Other symptoms include photosensitivity, decreased LOC, seizures. In infants, poor feeding, irritability. Outcome of bacterial meningitis worse than viral; bacterial has 5-50% mortalitly, viral is rarely fatal. Factors that affect outcome include age (worse in children, especially neonates), extent of infection, type of infection (bacterial vs viral, etc), amount of time elapsed before effective treatment is initiated. Common longterm effects: usually none with viral; with bacterial- deafness, MR, focal neuro deficits. |
| What are symptoms seen with meningitis- give classic triad then additional symptoms. Also give symptoms in infants. | Triad: fever, stiff neck (aka nuchal rigidity), headache- all more severe with bacterial. Additional symptoms: photosensitivity, nausea/vomiting, confusion/disorientation, decreased LOC, seizures. Symptoms in infants: fever, irritability, poor feeding, lethargy, vomiting, seizures. In meningococcal disease: abnormal colored skin rash. |
| What are the EEG changes in bacterial meningitis? Viral? | Bacterial meningitis: more abnormal in kids; moderate-severe diffuse slowing, irregular or intermittent rhythmic delta, +/- epileptiform. Viral: normal in >50%; more likely to me abnormal in kids, abnormalities are generally mild, diffuse nonspecific slowing, epileptiform rarely seen. |
| Is there a time when a cerebral lesion may not produce an abnormality on the EEG? If so, list possible cases where this might be true. | Yes- may occur if... 1. Lesion is too small 2. Lesion is too deep 3. Interictal abnormalities don’t occur within the 20-30minute EEG recording (ie. EEG is only a brief snap-shot of cerebral function) 4. Lesion is chronic and time from EEG to insult is long enough that abnormalities are no longer seen 5. Some lesions are known not to produce any abnormal findings |
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