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Neurological System > 3-CNS > Flashcards

3-CNS Flashcards

1
Q

Define seizure. Epilepsy

A

Abnormal synchronized discharge of neurons.
Electrical short circuit in the brain
6-10% of people have one seizure in their lifetime

Epilepsy - recurrent unprovoked seizures.

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2
Q

Describe generalized seizures.

A

Innitial presentation is non-lateralized. Despite the fact that the entire brain is affected at once. The generalized seizures come with a variety of symptoms.

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3
Q

What is the difference between tonic, atonic, and clonic seizures?

A

Tonic- Hypertonia
Atonic-Loss of consciousness
Clonic- generalized jerking of all 4 extremities

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4
Q

Difference between simple partial and complex partial seizures?

A

simple - NO alteration in consciousness

complex - alteration in consciousness

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5
Q

Describe the jerks of myoclonic seizures and what makes it different from clonic seizures/

A

Sudden, brief jerks

*no loss of consciousness

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6
Q

What is the most common location of origin of complex partial seizures?

A

Temporal lobe

Often have aura’s

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7
Q

Describe primary generalized epilepsy syndrome

A

Genetic
Neurologically normal
EEG shows epileptiform activity with normal background
Usualy easily controlled with anti-epileptics

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8
Q

Describe benign febrile convulsions.

A

Usually genetic
4 months to 4yrs
Generalized seizures
Occur at rapid rise of temp.

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9
Q

Treatment for benign febrile convulsions?

A

rectal valium(diastat)

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10
Q

6 yr old healthy girl w/ new onset starring spells. Stops mid sentence and is blank for about 15 secs. She is unaware of the spells and has no post-confusion. She has them all day long. What is it?

A

Childhood absence epilepsy

DOC - Ethosuxamide (valproic acid works well too)

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11
Q

Differentiate seizure, epilepsy, and status epilepticus.

A

Seizure: abnormal synchronized discharge of neurons (short circuit). Brief, stereotypical and paroxysmal.

Epilepsy: recurrent unprovoked seizures. Neonates and elderly.
Intractable epilepsy: not controlled by medication (20-40%).
Cause: multifactorial; genetic; trauma; developmental; stroke; idiopathic.

Status epilepticus: prolonged seizure (greater than 5 minutes); repeated seizures lasting more than 5 minutes. Medical emergency.
Diagnosis: EEG.
Cause: non-complience with medication; metabolic; trauma; drug/EtOH withdrawal; CNS infection.

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12
Q

Recall the prevalence and prognosis of each. Seizure

A

Seizure: 6-10% have one in lifetime.
Epilepsy: 1% population (3% lifetime risk).

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13
Q

Describe Tonic Clonic

A

Generalized. loss of consciousness; tonic (hypertonia; stiffening of axial/limb muscles; ictal cry); clonic (jerking of extremities).
Urinary incontinence (sphincter relax).
Postictal phase: stuporous/obtunded; deep sonorous respirations. Headache; diffuse myalgia.

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14
Q

Describe Absence

A

Generalized. sudden behavioral arrest (staring); may have automatisms; no postictal confusion; no aura. Exacerbated by hyperventilation.
EEG: generalized 3 hz spike and wave discharge.

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15
Q

Describe Atonic

A

Generalized: sudden loss of postural muscle tone (drop attacks); brief impaired consciousness; minimal postictal state.
EEG: low voltage fast activity, polyspike and wave; electrodecrement.

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16
Q

Describe Myoclonic

A

Generalized sudden brief jerks (UE [more common], LE, face; bilateral and symmetrical). Consciousness NOT impaired. No postisctal confusion.

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17
Q

Describe Simple partial seizure.

A

Partial. NO alteration in consciousness.

Features: depends on location (taste; smell; feeling; visual; clonic movement [Jacksonian march]; Todd paralysis.

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18
Q

Describe Complex Partial seizure.

A

alteration in consciousness. Partial. Most difficult seizure to control.
Features: aura (often); amnesia (hippocampus); temporal lobe most common; stop, stare, automatisms (oral buccal).

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19
Q

Describe partial with secondary generalization.

A

Partial. start focally then present as “Grand Mal”. Look for localizing factors (eye deviation, Todd paralysis).

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20
Q

Describe primary generalized epilepsy.

A

genetic (usually); neurologically normal.

EEG: epileptiform (spike wave discharge) with normal background.

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21
Q

Describe Benign febrile convulsions.

A

genetic (usually); 4 months to 4 years (kids).
Features: generalized seizures; occur at high temperatures (rapid rise).
Treatment: symptomatic; rectal valium (diastat; for prolonged seizure). Usually do NOT give antiepileptic drugs.

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22
Q

Describe childhood absence epilepsy.

A

“petite mal.” Onset 4-8 years.

Features: brief staring; no post ictal state; provoked by hyperventilation. Often “out grow.”

EEG: generalized 3 Hz spike and wave.

Treatment: ethosuxamide
(DoC); valproic acid.

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23
Q

Describe Juvenile Myoclonic epilepsy.

A

genetic.
Features: absence; myoclonic jerks; generalized tonic-clonic upon awakening.
Provoking factors: alcohol; photic stimulation; sleep deprivation.
EEG: generalized polyspike and wave.
Treatment: valproic acid (Depakote; DoC). May require chronic administration.

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24
Q

Symptomatic/Secondary Epilepsy Syndromes

A

acquired/idiopathic; neurologically abnormal; multiple seizure types; intractable to medication.
EEG: very abnormal (no normal background activity).

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25
Q

West syndrome:

A 
infantile spasms (extend arms; flex/bow).
EEG: hypsarrhythmia.
Features: severe developmental delay.
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26
Q

Lennox Gastaut syndrome

A

variable causes.
Features: multiple seizure types; mental retardation; developmental delay; intractable to medication.
EEG: slow spike and wave, multifocal spikes, paroxysmal fast activity.

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27
Q

Partial Epilepsy syndromes:

A

history of complicated febrile convulsions.
Features: intractable complex partial seizures.

MRI: mesial temporal sclerosis (results in abnormal signaling).

EEG: focal temporal slowing or spikes.

Treatment: temporal lobectomy (70% seizure free).

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28
Q

Recall the work up for seizures.

A

H&P (most important); neurological exam; blood/urine tests; EEG; MRI brain (check for lesion).

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29
Q

EEG for Absence seizure

A

generalized 3hz spike and wave discharge.

Childhood absence epilepsy.

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30
Q

EEG for Atonic

A

low voltage fast activity, polyspike and wave; electrodecrement.

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31
Q

EEG for Juvenile Myoclonic epilepsy:

A

generalized polyspike and wave.

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32
Q

EEG for Secondary epilepsy syndrome

A

very abnormal (no normal background activity).

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33
Q

EEG for West syndrome

A

hypsarrhythmia (highly disorganized).

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34
Q

EEG for Lennox Gastaut:

A

slow spike and wave, multifocal spikes, paroxysmal fast activity

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35
Q

EEG for Partial epilepsy syndromes

A

focal temporal slowing or spikes.

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36
Q

List treatments for epilepsy and status epilepticus.

A

Monotherapy is desireable.
ABCs.
IV benzodiazepine (lorazepam, diazepam); IV phenytoin/phosphenytoin; induced coma (IV phenobarbital/midazolam/propofol).
Find cause: blood work; CT; LP.

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37
Q

Differentiate auras, postictal confusion, Todd’s paralysis, and pseudoseizures.

A

Aura: early warning before a seizure (simple partial seizure).

Postictal confusion: stuperous or obtunded; deep sonorous respirations.

Todd paralysis: focal weakness of a part of the body after seizure (usually located to one side). May also affect speech, eye position, vision.

Pseudoseizures: psychogenic non-eplileptic attacks (PNEA). Difficult to distinguish from seizure. Lack of seizure EEG findings.

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38
Q

Discuss seizure safety issues with a patient.

A

No driving, bathing/swimming alone, unsupervised heights.

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39
Q

Tips for ped exam?

A

observe first (play games, watch them feed).
Visual acuity: observe reach for objects.
EOMs: use toys.
Corneal light reflex: eye alignment.
Red reflex.
Assess suck: pacifier, gloved finger.
Head lag: from supine to sitting; should only be slight.
Frog leg position: hypotonia.
Tone: predominant flexor tone is normal.

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40
Q

Stepping reflex

A

Birth- 2months

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41
Q

Galant reflex

A

Birth- 2 mos

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42
Q

Grasp reflex

A

Birth- 3 mos

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43
Q

Moro reflex

A

birth - 6 mos

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44
Q

Tonic Neck reflex

A

birth - 6 mos

45
Q

Root reflex

A

birth - 7 mos

46
Q

Babinski reflex

A

birth - 2 yrs

47
Q

Parachute reflex

A

persists

48
Q

When does the social smile start/recognize parents?

A

2 mos

49
Q

When can child roll front to back?

A

4 mos

50
Q

When can child foll back to front?

A

5 mos

51
Q

When can child sit unsupported, recognize strangers?

A

6 mos

52
Q

When can child walk alone, use more than mama/dada words?

A

12 mos

53
Q

Explain APGAR scoring.

A 
up to 10; each category rated 0-2. Scored at 1 and 5 minutes (10 and 15 if problems).
Appearance (color).
Pulse.
Grimace (reflex irritability).
Activity (muscle tone).
Respirations).
54
Q

Give examples of when you may see a positive Gower sign.

A

Gower sign: child must climb up legs to rise from crawl position. Proximal muscle weakness.
Positive: muscular dystrophy; myopathies.

55
Q

Inspect for floppy baby syndrome and list causes.

A

extreme head lag. ¾ due to ischemia or brain or cord, spinal muscular atrophy, dysgenetic syndromes.
Causes: brain, brainstem, spinal cord, peripheral nerve, neuromuscular junction, muscle, metabolic.

56
Q

Spinal muscular atrophy and its types? (3)

A

SMA 1: Werdnig Hoffman (onset birth; 80% die within 1 yr).

SMA 2: by 3 months.

SMA 3: Kugelberg Welander (infancy/early childhood onset; normal life span).

57
Q

Prepare families for complications from prematurity and extreme prematurity.

A

Prematuraty: < 37 weeks gestation. 1/3rd infant deaths in US.
Extreme prematurity: < 25 weeks gestation. 50% mortality.
Disabilities: motor deficits; cerebral palsy; vision/hearing loss; impaired cognitive skills; behavioral/psychological problems.

58
Q

Prematuraty:

A

< 37 weeks gestation. 1/3rd infant deaths in US.

59
Q

Extreme prematurity:

A

< 25 weeks gestation. 50% mortality.

60
Q

DDX for neonatal encephalopathy? what is it?

A

any CNS dysfunction in newborn period.

Causes: usually asphyxia/hypoxic.
Ischemic encephalopathy.
Perinatal stroke.
Metabolic/genetic

61
Q

TX for neonatal encephalopathy?

A

supportive (ventilation; metabolic); control seizures; therapeutic hypothermia (72 hours; only neuroprotective therapy).

62
Q

Summarize neonatal asphyxia.

A

Perinatal asphyxia: hypoxic (ischemic encephalopathy).
Before birth (20%); during labor (70%); after birth (10%).
Cause: umbilical

63
Q

Differentiate the types of IVH. (intraventricular hemorrhage) 4 types.

A

subependymal. < 32 week gestation; < 1500 g birth weight.
Cause: venous/arterial (arise in vascular germinal plate in region of caudate).

Type I: confined to matrix. Asymptomatic.

Type II: extends into lateral ventricle. Irritability, lethargy.

Type III: enlarges ventricles.

Type IV: in brain parenchyma. Apnea, bradycardia, opisthotonus, extensor posturing, brainstem findings (also type III).

64
Q

Describe dx and tx for IVH in neonates

A

Diagnosis: H&P; ultrasound (routine screening); CT; MRI; LP.

Treatment: supportive; preserve perfusion, minimize complications.

Prevention: prevent premature birth; antenatal corticosteroids; delayed clamping of umbilical cord (> 30 sec); prompt resuscitation.

65
Q

Neonatal intracranial hemorrhage:

A

Full term, large baby: subdural hematoma.
Premature (< 32 weeks): parenchymal.
Page 26 of 51 Clinical Neuro LO Exam 3
Full term: subarachnoid.
Risk factors: abnormal labor (forceps; vacuum extraction; C-section).

66
Q

Distinguish neonatal seizures.

A

Neonatal seizures: symptomatic of serious neurological disease. 15% mortality; 35-40% serious morbidity.

Cause: metabolic; infection; neonatal encephalopathy and IVH (1/3rd cases).

Features: unifocal/multifocal (jerking; rhythmic eye deviation; tonic posturing).

Diagnosis: H&P; EEG; determine underlying cause.
Treatment: underlying cause; phenobarbital; phenytoin; pyridoxine.

67
Q

Detect infantile botulism.

A

Infant botulism: ingestion of clostridial spores (raw honey; contaminated environmental dust). 1 week – 12 months.

Features: weakness; hypotonia; constipation; feeding difficulties; drooling; irritability.

68
Q

Differentiate types of cerebral palsy.

A

Types: spastic; dyskinetic; ataxic; mixed; atonic.
Spastic hemiparesis: thinner/smaller extremity; increased tone/reflexes.
Spastic tetraparesis: all four extremities; pseudobulbar (speech, swallowing, drooling).
Spastic diplegia: legs (more common than arms).
Dyskinetic: athetosis; chorea; dystonia. Involve basal ganglia. Kernicterus was a major cause in the past (jaundice).

69
Q

Describe cerebral palsy

A

nonprogressive disorder; multifactorial. Brain pathology.
Associated with prematurity: periventricular leukomalacia (white matter changes in periventricular areas).

Etiology: prematurity; asphyxia; hemorrhage; trauma; infection; multiple pregnancy; genetics.

Features: seizure; mental retardation; psychiatric disorders; speech/vision problems; orthopedic problems; urinary problems.

Risk reduction: antenatal administration of magnesium sulfate (reduce risk/severity of CP).

70
Q

What is SIDS?

A

Sudden infant death syndrome (SIDS): leading cause of infant mortality (1 month – 1 year) in US. Sudden death of infant < 1, which is unexplained after thorough investigation (complete autopsy; examination of scene; review of clinical history).

71
Q

Summarize risk factors for SIDS.

A

Risk factors: young maternal age (< 20); maternal smoking during pregnancy; late/no prenatal care; preterm/low birth weight; prone sleeping position; soft surface; overheating.

Risk reduction: sleep on back.

72
Q

Segmentation and cleavage:

A

holoprosencephaly; Klippel-Feil syndrome.

73
Q

Sulcation and neuronal migration

A

callosal agenesis; hetertopias; lissencephaly; macrogyria; schizencephaly; microgyria.

74
Q

What is craniosyntosis?

A

premature fusion of sutures.

75
Q

Scaphocephaly

A

sagittal suture fused early

76
Q

Brachycephaly

A

coronal sutures fused early

77
Q

Plagiocephaly

A

twisted skull. unilateral coronal or lamboidal syntosis

78
Q

Trigonocephaly

A

metopic suture closed early (pointed forehead)

79
Q

Complications of craniosyntosis?

A

increased ICP; inhibition of brain growth; cognitive and neurodevelopment problems; poor self-esteem; social isolation.

80
Q

Cloverleaf deformity (Kleeblattschadel):

A

multiple sutures. Most severe (hydrocephalus; mental retardation).

81
Q

ADHD DOC?

A

Methylphenidate

82
Q

Differentiate between the pervasive developmental disorders

A

Autism: 1/150 – 1/500. Male:female, 4:1. Symptoms must be present by 3 yo.
Features: impaired social interaction; impaired communication (does not attain or regresses); restricted/repetitive/stereotyped patterns of behavior; increased rate of head growth; aberrant sensory processing abilities (42-99%).
Deviant behavior: infrequent cry; does not want to be held; unusually good; plays by self; absent smiling; withdraws from presence of others.
Regressive: develop normally age 18-24 months.
Absorbing interests and ritualistic behavior: disruption causes rage/tantrum.

Asperger syndrome: “milder” autism. Better verbal expression; higher level of cognitive function.

Pervasive developmental disorder NOS: have some, not all criteria for diagnosis of autism or Asperger.

Rett syndrome: MECP2 gene mutation (methylcytosine binding protein; X chromosome). Early mortality in boys (almost exclusively females).
Features: dementia; stereotypic hand movements; deceleration of head growth.

83
Q

Define MR and discuss etiologies.

A

Intellectual Disability/Mental Retardation: limited intelligence; adaptive functioning impairment; begins in childhood. Static encephalopathy. IQ < 100. 1-3% of population (85% mild).

Cause: multiple etiologies.

Genetic: Fragile X syndrome; Down syndrome; Rett syndrome.

Preterm birth; hypoxia; intracranial hemorrhage; postnatal trauma; hypoxia; toxins; malnutrition; infection; psychosocial deprivation.

Metabolic: PKU, hypothyroidism, hydrocephalus.

84
Q

Larges features of MR?

A

global developmental delay; impairment of adaptive function.

85
Q

Global developmental delay def.

A

Term used to describe children with Intellectual disability younger than age 5. IQ testing is unreliable in this age group

86
Q

What does DSM IV stand for?

A

Diagnostic and Statistical Manual of Mental Disorders

Uses the term mental retardation defined as:

(significant sub-average intellectual function; significant limitations in adaptive functioning; onset before 18 years).

87
Q

What are the levels of MR?

A

Mild: IQ 50-70.
Moderate: 35-50.
Severe: 20-35.
Profound: < 20.

88
Q

Common causes of inherited/born MR?

A

Fragile X Syndrome: 1-2% MR. Most common inherited cause. Trinucleotide expansion. Females (fewer/milder abnormalities). Long faces; large ears; macroorchidism.

Fetal alcohol syndrome: common cause of MR. Poor growth; CNS abnormalities; dysmorphic facial features.

89
Q

Be able to recognize common clinical features in MR cases.

A

Global developmental delay; impairment of adaptive function.
13-50% vision disorders.
~18% hearing impairments.

90
Q

Neurofibromatosis:

A

NF1: chromosome 17 (neurofibromin). Von Recklinghausen disease.

NF2: chromosome 22 (neurofibromin 2; schwannomin; merlin). Bilateral acoustic neuromas. Mild cutaneous changes.

91
Q

Features of Neurofibromatosis

A

café-au-lait spots (> six, > 5 mm prepubertal; > 15 mm postpubertal); axiallary/inguinal freckling; neurofibromas; lisch nodules (NF1; iris hamartomas); learning disabilities; seizures; macrocephaly.

92
Q

Sturge Weber:

A

trigeminocranial angiomatosis (cerebal calcification).

Features: facial port wine (nevus flammeus); leptomeningeal angiomatosis; seizures (refactory); MR; contralateral hemiparesis; glaucoma.

Imaging: atrophy and calcification in occipital lobe (“trolley track”; curvilinear).

Risk: nevus flammeus over entire ophthalmic area (glaucoma; neurologic complications).

93
Q

Tuberous sclerosis

A 
chromosome 9 (hamartin) and 16 (tuberin).
Triad: MR; epilepsy; skin lesions (adenoma sebaceum; looks like acne)

Features: infantile spasms (hypsarrhythmia); hamartomas; ash leaf hypopigmented macules (skin lesions present from birth; may need Wood lamp); subungual fibroma; shagreen patch (subepidermal fibrous patches); café-au-lait spots; subependymal nodules.

94
Q

Differentiate PKU, MSUD, and Homocystinuria

A

Phenylketonuria (PKU): autosomal recessive. 1/10,000.
Pathology: deficient phenylalanine hydroxylase (phenylalanine  tyrosine). Phenylalanine accumulates (converted to organic acid). Defective demyelination; decreased pigmentation.
Features: vomiting, irritability (first 2 months); delayed development; MR; seizures; infantile spasms; tremors (~35%).
Blond, blue eyed, eczema; “musty” odor.
Diagnosis: H&P; newborn screening.
Treatment: dietary (restrict phenylalanine).

Maple Syrup Urine Disease (MSU):
Pathology: disorder of branched chain amino acid metabolism (valine, leucine, isoleucine).
Features: opsithotonos; hypertonia; seizures; hypoglycemia. Urine/perspiration smells like sweet maple syrup.
Treatment: diet (restrict BCAA).

Homocystinuria: autosomal recessive.
Pathology: error of methionine metabolism.
Features: seizure; developmental slowing (MR); ectopia lentis (dislocation of lens); multiple thromboembolic events (risk for stroke).

95
Q

Describe Lesch- Nyhan Syndrome.

A

X-linked.
Pathology: hypoxanthine-guanine phsphoribosyltransferase (HPRT) deficiency.
Features: hyperuricemia; MR; spasticity; choreoathetosis; self-mutilation (painful uric acid deposits); death (chronic renal failure).

96
Q

Differentiate Tay Sachs and Niemann Pick.

A

Tay-Sachs: hexosaminidase A deficiency.
Features: myoclonic jerks; cherry red spot (macula); floppy baby; hyperreflexia; clonus; Babinski; seizures; enlarged head.
Prognosis: death from infection.

Niemann-Pick: sphingomyelinase deficiency.
Features: hepatosplenomegaly; developmental regression; dementia; hypotonia; cherry red spot.
Diagnosis: bone marrow biopsy; deficiency of sphingomyelinase in leukocytes/skin fibroblasts.

97
Q

Detect Wilson Dz.

A

hepatolenticular degeneration. Autosomal recessive. Onset 11-25 years.
Pathology: mutation ATP7B (chromosome 13).

Accumulation of copper.

Sequelae: cirrhosis of liver; degenerative changes in basal nuclei.

Features: jaundice; ascites; tremor (resting; intention; wing-beating); rigidity; dystonia; Kayser-Fleischer rings (75% hepatic; 100% cerebral cases); psychiatric symptoms; seizures.

Diagnosis: H&P (family history); lab (liver function; urine [copper]; serum ceruloplasmin level [reduced]); liver biopsy; MRI brain.

Treatment: remove copper and prevent accumulation.
D-pneicillamine, trientine, oral zinc, ammonium tetrathiomolybdate.
Diet: low copper.
Liver transplant.

98
Q

Discuss dizziness in the elderly.

A 
High prevalence (up to 38%).
Risk of fall (disability; institutionalization; death).
Vision impairment: exacerbates it. “Multiple sensory defect dizziness.”
99
Q

Define vertigo, and distinguish with presyncope.

A

Vertigo: false sensation of movement. Dysfunction of vestibular system.
Provoking factors: change in head position; middle ear pressure.

Presyncope: near fainting; lightheadedness; warmth; diaphoresis; nausea; visual blurring; pallor; when standing/sitting.
Dysrhtyhmias; CAD; CHF; palpitations; chest discomfort; dyspnea; heart disease.

100
Q

Distinguish central versus peripheral vertigo by symptomology and nystagmus.

A

Central vertigo: involve brainstem or cerebellum.
Nystagmus: immediate or delayed; no habituation. Horizontal/rotary/vertical (may change directions).
Neurological deficits: typically present

Peripheral vertigo: inner ear.
Nystagmus: delayed; habituates. Not vertical (does not change directions).
Fast phase: toward normal ear.
Hearing loss or tinnitus.

101
Q

most common cause of vertigo.

A

Benign paroxysmal positional vertigo (BPPV):

Features: aggravated by head movement.

Vertigo: seconds; nausea (rarely vomit). Repeated, brief episodes that continue for weeks/months, may recur.

Nystagmus: rotatory; fatiguable; transient.

Cause: trauma; idiopathic.
Pathophysiology: canalithiasis (otoliths dislodged).

Diagnosis: Dix-Hallpike (50-80%).

Treatment: canalith repositioning; medication; adaptation; surgery.

102
Q

Meniere disease:

A

Features: vertigo (severe, spontaneous, episodic; minutes to hours); unilateral tinnitus; deafness (progressive and stepwise); sensitive to sounds; pressure feeling; distorted sounds; nausea, vomiting, imbalance.

Cause: increase in endolymphatic volume (endolymphatic hydrops).

Treatment: restrict salt; diuretics; surgery.

103
Q

Vestibular Neuritis

A

lasts days; may recur for months.

Features: vertigo (sudden, severe); nausea, vomiting, gait instability.

Labyrinthitis: with unilateral hearing loss.

Pathology: affects vestibular portion of CN VIII.

Treatment: conservative; medication (corticosteroid).
Imaging: rule out CVA or hemorrhage.

104
Q

Ramsay Hunt syndrome

A

reactivation of herpes zoster virus in ear.

Features: acute vertigo, hearing loss; ipsilateral face palsy; ear pain, vesicles.

105
Q

Know the pharmacologic and non pharmacologic treatments of vertigo

A

Antihistamines: meclizine; promethazine; dimenhydrinate.

Anticholinergics: scopolamine.

Benzodiazepines: diazepam.

106
Q

Interpret findings from Dix-Hallpike testing.

A

Dix-Hallpike maneuver: patient sitting. Examiner supports head as patient lies back, head turned so one ear down, repeat on other side.
Positive: subjective sense of vertigo; objective finding of nystagmus.
Peripheral disorder: latent period before onset (2-20 sec); duration (< 1 min); fatigueability; direction (only one); vertigo (severe).
Central disorder: no latent period; duration (> 1 min); nonfatiguing; direction (may change); vertigo (less severe; maybe none).

107
Q

Differentiate types of syncope (4)

A

Vasovagal syncope: decreased pulse or blood pressure in response to triggering event (pain; emotion; unpleasant experience). Lasts few minutes (rapid recovery).
Treatment: conservative.

Orthostatic hypotension: change in posture.
Associations: medication; viral infection; bed rest; dehydration; anemia; adrenal insufficiency.
Etiology: diabetes mellitus; syrinx; syphilis; Shy-Drager syndrome; idiopathic.
Diagnosis: tilt test (BP drops > 20 mmHg systolic/10 mmHg diastolic; heart rate increases 11-29 bpm).

Carotid sinus syncope: unusual carotid sinus sensitivity (pressure on neck; tight collar). Elderly. Decrease pulse/BP.
Diagnosis: ECG monitoring with light massage to neck.

Convulsive Syncope: seizure triggered by rapid decline in BP.

108
Q

Differentiate seizure from syncope.

A

Syncope: postural, rapid recovery

Seizure: slow recovery, frequent incontinence

Neurological System (10 decks)

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