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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
West syndrome:
``` infantile spasms (extend arms; flex/bow). EEG: hypsarrhythmia. Features: severe developmental delay. ```
26
Lennox Gastaut syndrome
variable causes. Features: multiple seizure types; mental retardation; developmental delay; intractable to medication. EEG: slow spike and wave, multifocal spikes, paroxysmal fast activity.
27
Partial Epilepsy syndromes:
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).
28
Recall the work up for seizures.
H&P (most important); neurological exam; blood/urine tests; EEG; MRI brain (check for lesion).
29
EEG for Absence seizure
generalized 3hz spike and wave discharge. | Childhood absence epilepsy.
30
EEG for Atonic
low voltage fast activity, polyspike and wave; electrodecrement.
31
EEG for Juvenile Myoclonic epilepsy:
generalized polyspike and wave.
32
EEG for Secondary epilepsy syndrome
very abnormal (no normal background activity).
33
EEG for West syndrome
hypsarrhythmia (highly disorganized).
34
EEG for Lennox Gastaut:
slow spike and wave, multifocal spikes, paroxysmal fast activity
35
EEG for Partial epilepsy syndromes
focal temporal slowing or spikes.
36
List treatments for epilepsy and status epilepticus.
Monotherapy is desireable. ABCs. IV benzodiazepine (lorazepam, diazepam); IV phenytoin/phosphenytoin; induced coma (IV phenobarbital/midazolam/propofol). Find cause: blood work; CT; LP.
37
Differentiate auras, postictal confusion, Todd’s paralysis, and pseudoseizures.
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.
38
Discuss seizure safety issues with a patient.
No driving, bathing/swimming alone, unsupervised heights.
39
Tips for ped exam?
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.
40
Stepping reflex
Birth- 2months
41
Galant reflex
Birth- 2 mos
42
Grasp reflex
Birth- 3 mos
43
Moro reflex
birth - 6 mos
44
Tonic Neck reflex
birth - 6 mos
45
Root reflex
birth - 7 mos
46
Babinski reflex
birth - 2 yrs
47
Parachute reflex
persists
48
When does the social smile start/recognize parents?
2 mos
49
When can child roll front to back?
4 mos
50
When can child foll back to front?
5 mos
51
When can child sit unsupported, recognize strangers?
6 mos
52
When can child walk alone, use more than mama/dada words?
12 mos
53
Explain APGAR scoring.
``` 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
Give examples of when you may see a positive Gower sign.
Gower sign: child must climb up legs to rise from crawl position. Proximal muscle weakness. Positive: muscular dystrophy; myopathies.
55
Inspect for floppy baby syndrome and list causes.
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
Spinal muscular atrophy and its types? (3)
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
Prepare families for complications from prematurity and extreme prematurity.
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
Prematuraty:
< 37 weeks gestation. 1/3rd infant deaths in US.
59
Extreme prematurity:
< 25 weeks gestation. 50% mortality.
60
DDX for neonatal encephalopathy? what is it?
any CNS dysfunction in newborn period. Causes: usually asphyxia/hypoxic. Ischemic encephalopathy. Perinatal stroke. Metabolic/genetic
61
TX for neonatal encephalopathy?
supportive (ventilation; metabolic); control seizures; therapeutic hypothermia (72 hours; only neuroprotective therapy).
62
Summarize neonatal asphyxia.
Perinatal asphyxia: hypoxic (ischemic encephalopathy). Before birth (20%); during labor (70%); after birth (10%). Cause: umbilical
63
Differentiate the types of IVH. (intraventricular hemorrhage) 4 types.
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
Describe dx and tx for IVH in neonates
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
Neonatal intracranial hemorrhage:
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
Distinguish neonatal seizures.
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
Detect infantile botulism.
Infant botulism: ingestion of clostridial spores (raw honey; contaminated environmental dust). 1 week – 12 months. Features: weakness; hypotonia; constipation; feeding difficulties; drooling; irritability.
68
Differentiate types of cerebral palsy.
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
Describe cerebral palsy
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
What is SIDS?
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
Summarize risk factors for SIDS.
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
Segmentation and cleavage:
holoprosencephaly; Klippel-Feil syndrome.
73
Sulcation and neuronal migration
callosal agenesis; hetertopias; lissencephaly; macrogyria; schizencephaly; microgyria.
74
What is craniosyntosis?
premature fusion of sutures.
75
Scaphocephaly
sagittal suture fused early
76
Brachycephaly
coronal sutures fused early
77
Plagiocephaly
twisted skull. unilateral coronal or lamboidal syntosis
78
Trigonocephaly
metopic suture closed early (pointed forehead)
79
Complications of craniosyntosis?
increased ICP; inhibition of brain growth; cognitive and neurodevelopment problems; poor self-esteem; social isolation.
80
Cloverleaf deformity (Kleeblattschadel):
multiple sutures. Most severe (hydrocephalus; mental retardation).
81
ADHD DOC?
Methylphenidate
82
Differentiate between the pervasive developmental disorders
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
Define MR and discuss etiologies.
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
Larges features of MR?
global developmental delay; impairment of adaptive function.
85
Global developmental delay def.
Term used to describe children with Intellectual disability younger than age 5. IQ testing is unreliable in this age group
86
What does DSM IV stand for?
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
What are the levels of MR?
Mild: IQ 50-70. Moderate: 35-50. Severe: 20-35. Profound: < 20.
88
Common causes of inherited/born MR?
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
Be able to recognize common clinical features in MR cases.
Global developmental delay; impairment of adaptive function. 13-50% vision disorders. ~18% hearing impairments.
90
Neurofibromatosis:
NF1: chromosome 17 (neurofibromin). Von Recklinghausen disease. NF2: chromosome 22 (neurofibromin 2; schwannomin; merlin). Bilateral acoustic neuromas. Mild cutaneous changes.
91
Features of Neurofibromatosis
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
Sturge Weber:
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
Tuberous sclerosis
``` 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
Differentiate PKU, MSUD, and Homocystinuria
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
Describe Lesch- Nyhan Syndrome.
X-linked. Pathology: hypoxanthine-guanine phsphoribosyltransferase (HPRT) deficiency. Features: hyperuricemia; MR; spasticity; choreoathetosis; self-mutilation (painful uric acid deposits); death (chronic renal failure).
96
Differentiate Tay Sachs and Niemann Pick.
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
Detect Wilson Dz.
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
Discuss dizziness in the elderly.
``` High prevalence (up to 38%). Risk of fall (disability; institutionalization; death). Vision impairment: exacerbates it. “Multiple sensory defect dizziness.” ```
99
Define vertigo, and distinguish with presyncope.
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
Distinguish central versus peripheral vertigo by symptomology and nystagmus.
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
most common cause of vertigo.
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
Meniere disease:
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
Vestibular Neuritis
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
Ramsay Hunt syndrome
reactivation of herpes zoster virus in ear. Features: acute vertigo, hearing loss; ipsilateral face palsy; ear pain, vesicles.
105
Know the pharmacologic and non pharmacologic treatments of vertigo
Antihistamines: meclizine; promethazine; dimenhydrinate. Anticholinergics: scopolamine. Benzodiazepines: diazepam.
106
Interpret findings from Dix-Hallpike testing.
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
Differentiate types of syncope (4)
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
Differentiate seizure from syncope.
Syncope: postural, rapid recovery Seizure: slow recovery, frequent incontinence

Neurological System (10 decks)

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