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Brain Power: Adam and Victor's Neurology > Developmental Diseases of the Nervous System > Flashcards

Developmental Diseases of the Nervous System Flashcards

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1
Q

Hydranencephaly is hydrocephalus + ?

A

HCP + destruction or failure of development of parts of the cerebrum

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2
Q

A focal developmental defect in the wall of the cerebral mantle that is due to the localized failure of evagination is _______

A

Schizencephaly

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3
Q

Differentiate macrocephlay from macroencephaly.

A

Macrocephaly is enlargement of the head
Macroencephaly is a subtype characterized by a large head with normal or only slightly enlarged ventricles indivative of advancing metabolic disease like Alexander, Canavan and Tay sachs disease

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4
Q

The following neuroradiologic terms all pertain to what pathology: moose head, race car and bat wing

A

Corpus callosum agenesis

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5
Q

What kind of craniostenoses results from affected:

  1. Lambdoid and coronal sutures
  2. Sagittal suture
  3. Coronal suture
A
  1. Lambdoid and coronal sutures: tower skull, oxycephaly, turricephaly, acrocephaly
  2. Sagittal suture: scaphocephalic long and narrow head
  3. Coronal suture: Brachycephalic, wide and short head
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6
Q

When the maximum length of the skull is in the diagonal plane rather than the sagittal plane what type of craniosynostosis results?

A

Plagiocephaly

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7
Q

What tumor has a tigroid appearance on MRI?

A

Lhermitte-Duclos type of cerebellar gangliocytoma

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8
Q

What disorder of neuronal migration results from the mutation of the following genes:

  1. SHH
  2. TSC1 (hamartin) and 2 (tuberin)
  3. FCMD (fukutin)
A
  1. SHH: Holoprosencephaly, Lissencephaly
  2. TSC1 (hamartin) and 2 (tuberin): Tuberous sclerosis, heterotropia
  3. FCMD (fukutin): Fukuyama muscular dystrophy, heteroropia– will also have cobblestone lissencephaly
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9
Q

What are prenatal markers of anencephaly?

A

Elevated alpha fetoprotein and acetylcholinesterase in the amniotic fluid at 15-16 weeks

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10
Q

What would the brain of baby with one eye and no nose look like?

A

Holoprosencephaly– two cerebral hemispheres form a single telencephalic mass

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11
Q

What are the components of the Dandy walker syndrome?

A
  1. Cystic enlargement of the 4th ventricle
  2. Vermian hypoplasia
  3. +/- HCP
  4. +/- agenesis of the corpus callosum with cortical dysgenesis
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12
Q

RELN mutation causes lissencephaly with?

A

Cerebellar hypoplasia

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13
Q

ARX mutation is assocaited with X linked lissencephaly and?

A

Agenesis or the corpus callosum and hypogonadism

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14
Q

What are the 3 diseases associated with a cobblestone brain? Nodularity of the pial surface.

A
  1. Fukuyama musular dystrophy fukutin
  2. Muscle eye brain disease POMGNT1 gene
  3. Walker Warburg syndrome
    (Lissencephaly, cortex, meninges and eyes fail to differentiate normally) POMT1 gene

All genes are for glycosyltransferase

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15
Q

What syndrome?

Craniofacial dysostosis, proptosis with shallow orbits, midline facial hypoplasia and short upper lip, malformed auditory canals and ears, moderate mental retardation

A

Crouzon syndrome

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16
Q

What type of dwarfism?

  1. AD, Hemihypertrophy
  2. Bird head, severe retardation , RAD3-realted protein mutation
  3. AR, DHCR7 mutation, microcephaly, ptosis, hypospadias
  4. AD, CREB binding protein defect, Grimacing smile, cataracts
  5. Generalized hirsutism and synophrys (eyebrows that meet across midline)
A
  1. AD, Hemihypertrophy: Russel silver syndrome
  2. Bird head, severe retardation , RAD3-realted protein mutation: Nanocephalic dwarphism
  3. AR, DHCR7 mutation, microcephaly, ptoris, hypospadias: Smith Lemli Opitz syndrome
  4. AD, CREB binding protein defect, Grimacing smile, cataracts: Rubinstein Taybi syndrome
  5. Generalized hirsutism and synophrys (eyebrows that meet across midline): De lange syndrome
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17
Q

When does the fusion of dorsal midline structures of the primitive neural tube take place?

A

First 3 weeks of post conceptional life

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18
Q

What is an eventration of brain tissue and its coverings through an unfused midline defect in the skull?

A

Encephalocoele

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19
Q

Differentiate spina bifida occulta VS meningocoele VS meningomyelocoele

A

SBO: cord inside canal, no external sac, subcutaneous lipoma or dimple or wisp of hair
Meningocoele: Dura and arachnoid protrusion
Meningomyelocoele: cord with the cauda equina is extruded

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20
Q

Unexplained meningitis with a tuft of hair at the back should prompt search for?

A

Sinus tract

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21
Q

What are the three most consistent anomalies that are associated with a Chiari Malformation?

A
  1. Extension of the tongue of cerebellar tissue posterior to the medulla and cord that extends into the cervical spinal canal
  2. Caudal displacement of the medulla and inferior part of the 4th ventricle into the cervical canal
  3. Frequent but not invariable association with syringomyelia or a spinal developmental abnormality
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22
Q 
Describe the details of the different types of chiari malformation:
Type 1
Type 2
Type 3
Type 4
A

Type 1: Cerebellar descent without meningomyelocele
Type 2: Cerebellomedullary descent with meningomyelocele
Type 3: High cervical or occipito cervical meningomyelocoele with cerebellar herniation
Type 4: Cerebellar hypoplasia

Type 0: no descent just “full” posterior fossa but with sxs
Type 1.5: Cerebellar descent with additional caudal brainstem displacement

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23
Q

What is them most common form of inherited mental retardation?

A

Fragile X syndrome

Affected individuals usually have delayed development of speech and language by age 2. Most males with fragile X syndrome have mild to moderate intellectual disability, while about one-third of affected females are intellectually disabled. Children with fragile X syndrome may also have anxiety and hyperactive behavior such as fidgeting or impulsive actions. They may have attention deficit disorder (ADD), which includes an impaired ability to maintain attention and difficulty focusing on specific tasks. About one-third of individuals with fragile X syndrome have features of autism spectrum disorders that affect communication and social interaction. Seizures occur in about 15 percent of males and about 5 percent of females with fragile X syndrome.

Most males and about half of females with fragile X syndrome have characteristic physical features that become more apparent with age. These features include a long and narrow face, large ears, a prominent jaw and forehead, unusually flexible fingers, flat feet, and in males, enlarged testicles (macroorchidism) after puberty.

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24
Q

Identify which chromosomal dysgeneses is involved:

  1. Trisomy 13: death in childhood
  2. Trisomy 18: death at infancy
  3. Abnormal cry like a kitten, severe mental retardation, micrognathia
  4. XXY: Males with sparse facial and body hair, gynecomastia, small testicles
  5. XO: Female Webbed neck, short stature, mild dev delay
  6. Marked dilation of the occipital horns of the lateral ventricles with thickening of the overylying rim of cortical gray matter and thinning of white matter– spasticity, seizures– mosaicism for trisomy 8
A
  1. Patau Trisomy 13: death in childhood– ndividuals with trisomy 13 often have heart defects, brain or spinal cord abnormalities, very small or poorly developed eyes (microphthalmia), extra fingers or toes, an opening in the lip (a cleft lip) with or without an opening in the roof of the mouth (a cleft palate), and weak muscle tone (hypotonia).
  2. Edwards Trisomy 18: death at infancy– Affected individuals may have heart defects and abnormalities of other organs that develop before birth. Other features of trisomy 18 include a small, abnormally shaped head; a small jaw and mouth; and clenched fists with overlapping fingers
  3. Cri-cu di chat syndrome Deletion in short arm of chromosome 5: Abnormal cry like a kitten, severe mental retardation, micrognathia
  4. Klinefelter syndrome: XXY: Males with sparse facial and body hair, gynecomastia, small testicles
  5. Turner syndrome: XO: Female Webbed neck, short stature, mild dev delay
  6. Colpocephaly: Marked dilation of the occipital horns of the lateral ventricles with thickening of the overylying rim of cortical gray matter and thinning of white matter– spasticity, seizures– mosaicism for trisomy 8
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25
Q

Identify which chromosomal dysgeneses is involved:

  1. Unstable repeat sequence in the CGG of X chromosome: Most common inherited form of dev delay, 1 in 1500 male births, 10% with severe dev delay, enlarged testes
  2. Combination of cerebral maldevelopement with cardiovascular abnormalities like supravalvular aortic stenosis traced to a microdeletion on chromosome 7
  3. At the first year, dev delay, obesity, hyperphagia, hypogonadism deletion in 15q11-q13
  4. Maternally inherited single gene defect, dev delay, inappropriate laughter, microcephaly, long tongue, thin upper lip,: HAPPY PUPPET SYNDROME
  5. Dominant defect on X chromosome, at 6-18 months slow steady regression in motor skills and mental abilities
A

Identify which chromosomal dysgeneses is involved:

  1. FRAGILE X SYNDROME Unstable repeat sequence in the CGG of X chromosome: Most common inherited form of dev delay, 1 in 1500 male births, 10% with severe dev delay, enlarged testes
  2. WILLIAMS SYNDROME Combination of cerebral maldevelopement with cardiovascular abnormalities like supravalvular aortic stenosis traced to a microdeletion on chromosome 7
  3. PRADER WILLI SYNDROME At the first year, dev delay, obesity, hyperphagia, deletion in 15q11-q13
  4. ANGELMAN SYNDROME Maternally inherited single gene defect, dev delay, inappropriate laughter, microcephaly, long tongue, tuhin upper lip,: HAPPY PUPPET SYNDROME
  5. RETT SYNDROME Dominant defect on X chromosome, at 6-18 months slow steady regression in motor skills and mental abilities
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26
Q

What is H3O mnemonic for prader willi syndrome

A

Hypomentia, hypotonia, hypogonadism, obesity

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27
Q

What is the teratogenic risk of AEDs in the general population?

A

3%

Those on AEDs approximately 5%

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28
Q

What are the 2 true phakomatoses?

A
  1. Tuberous sclerosis

2. Neurofibromatosis

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29
Q

What is the triad of tuberous sclerosis?

A
  1. Adenoma sebaceum: angiofibromas in the face (aka adenomas of Pringle)
  2. Epilepsy
  3. Developmental delay
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30
Q

What chromosomes are TSC 1 hamartin and TSC 2 tuberin located in?

A

TSC 1: Hamartin in (9q long arm)

TSC 2: Tuberin in (16 p short arm)

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31
Q

What is the initial seizure pattern of tuberous sclerosis?

A

In the first year or two they take the form of massive flexion spasms with hypsarrhythmia –> GTC and psychomotor attacks or petit mal

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32
Q

What is a phakoma?

A

A gliomatous tumor in the retina in or near the optic disc

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33
Q

If adenomas of Pringle are found in the face what diagnostic lesion of tuberous sclerosis is found in the trunk?

A

shagreeen patch

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34
Q

What are cortical tubers made up of?

A

plump fibrous astrocytes much like astrocytoma though lacking in glial fibrillar protein

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35
Q

What AED can be used for the flexor spasms of tuberous sclerosis at infancy? How about status epilepticus associated with TS?

A

ACTH

Everolimus– DON’T FORGET THIS!

36
Q

Molluscum fibrosum (non-neural skin tumors) of NF is distinguished from lipomas by the phenomenon of?

A

“buttonholing”

37
Q

What is a Lisch nodule?

A

small whitish spot representing an iris hamartoma

38
Q

Diagnostic criteria for Tuberous sclerosis?
__ Major
__ Major + __ Minor

Besides shagreen patch, ash leaf spots 3 or more, cortical dysplasias more than 3, SEGA what are the other major signs

A

2 major
1 major 2 minor

Major:

Angiofibromas (3 or more) or forehead plaque
Hypomelanotic macules “ash leaf spots” (3 or more)
Ungual fibromas (2 or more)
Shagreen patch or multiple collagenomas
Multiple retinal hamartomas
Cortical dysplasias (more than 3). This includes tubers and cerebral white matter radial migration lines.
Subependymal nodule(s)
Subependymal giant cell astrocytoma(s)
Cardiac rhabdomyoma
Lymphangioleiomyomatosis (LAM)
Angiomyolipomas (2 or more)

Minor:

Dental enamel pits (more than 3)
Intraoral fibromas (2 or more)
Nonrenal hamartomas
Retinal achromic patch
“Confetti” skin lesions
Multiple renal cysts
39
Q

How to diagnose NF1?

A

Clinical diagnosis based on presence of two of the following:

  1. Six or more café-au-lait macules over 5 mm in diameter in prepubertal individuals and over 15mm in greatest diameter in postpubertal individuals.
  2. Two or more neurofibromas of any type or one plexiform neurofibroma.
  3. Freckling in the axillary or inguinal regions.
  4. Two or more Lisch nodules (iris hamartomas).
  5. Optic glioma.
  6. A distinctive osseous lesion such as sphenoid dysplasia or thinning of long bone cortex, with or without pseudarthrosis.
  7. First-degree relative (parent, sibling, or offspring) with NF-1 by the above criteria.

Diagnostic criteria CAFE SPOt:[2]
Café-au-lait spots. Six or more. 5mm/15mm
Axillary or inguinal freckling.
neuroFibroma (two or more) or plexiform neurofibroma (one).
Eye hamartomas (Lisch nodules). 2 or more
Skeletal abnormalities, e.g. sphenoid dysplasia, leg bowing.
Positive family history. or Pamily (hehe)
Optic Nerve Tumour (optic nerve glioma).

40
Q

What percentage of NF1 patients can be diagnosed with the presence of 6 or more cafe au lait spots?

A

80%

41
Q

How to diagnose NF2?

A

Confirmed (definite) diagnosis of NF2:

bilateral vestibular schwannomas (may also be known as acoustic neuroma)
(Probable) diagnosis of NF2:

family history of NF2 AND
unilateral vestibular schwannomas or any 2 of the following tumor types: meningioma, glioma, schwannoma, juvenile posterior subcapsular lenticular opacity, juvenile cortical cataract

Mnemonic MESE2 (Meningioma, Ependysmoma, Schwannoma, Cataract, Lens opacity)

42
Q

What ocular pathology is associated with NF2?

A

posterior subcapsular lenticular opacity, juvenile cortical cataract

43
Q

What orthopedic pathology is associated with NF1?

A

A distinctive osseous lesion such as sphenoid dysplasia or thinning of long bone cortex, with or without pseudarthrosis.v

44
Q

Meningo-Encephalofacial angiomatosis with cerebral calcification is aka?

A

Sturge weber syndrome

45
Q

The vascular nevus in sturge weber synrome is usually located in what part of the face?

A

Ophthalmic division

46
Q

The calcifications seen in Sturge weber syndrome is seen in in what layer of the cortex?

A

2nd and third
2nd external granular
3rd external pyramidal

47
Q

For sturge weber syndrome what pathologies are found in the:

  1. Brain
  2. Eye
A
  1. Leptomeningeal angioma and calcifications

2. Glaucoma and facial angioma surrounding the eye

48
Q

Hereditary hemorrhagic telangiectasia is AKA

A

Osler Rendu Weber Disease

49
Q

What are the key features of von Hippel lindau? VHL gene on chromosome 3

A
  1. Hemangioblastoma in the cerebellum, brainstem or spinal cord
  2. Retinal hemangioblastoma
  3. Renal Cell CA 60% of patients with 1/3 mortalities
  4. Polycythemia vera
  5. Pheochromocytoma
  6. Pancreatic tumors
50
Q

What are the characteristic locations of telangiectasias in ataxia telangiectasia syndrome (AR)?

A

Outer parts of the bulbar conjunctivae (early) and over the years on exposed parts of the neck, on the bridge of the nose and cheeks

51
Q

How do patients with ataxia telangiectasia syndrome die?

What is another name for the Ataxia telangiectasia? How is it inherited? What chromosome and arm is involved?

A

Usually from bronchopulmonary infection or neoplasia due to humoral immunodeficiency decrease in IgA IgE IgG2 IgG4

Louis Bar syndrome. AR. 11q long arm

52
Q

Why are patients with ataxia telangiectasia syndrome at risk for post radiation lymphoma, leukemia and other tumors?

A

Mutations in the ATM gene cause ataxia-telangiectasia. The ATM gene provides instructions for making a protein that helps control cell division and is involved in DNA repair. This protein plays an important role in the normal development and activity of several body systems, including the nervous system and immune system. The ATM protein assists cells in recognizing damaged or broken DNA strands and coordinates DNA repair by activating enzymes that fix the broken strands. Efficient repair of damaged DNA strands helps maintain the stability of the cell’s genetic information.

Mutations in the ATM gene reduce or eliminate the function of the ATM protein. Without this protein, cells become unstable and die. Cells in the part of the brain involved in coordinating movements (the cerebellum) are particularly affected by loss of the ATM protein. The loss of these brain cells causes some of the movement problems characteristic of ataxia-telangiectasia.

53
Q

What are the two main symptoms that comprises Mobius syndrome? What are the others

A

Facial Diplegia and abducens palsies

Lingual palsy
Clubfeet
Complete ophthalmoplegia
Clubfeet
Mental defect
Absent pectoral muscle
54
Q

Describe the findings in Cogan’s oculomotor apraxia.

A

Lack of lateral gaze volitionally or on command– responds to caloric stimulation

55
Q

In those born from 20-35W fatal brain bleeds can usually be found in what area?

A

Subependymal germinal matrix zone near the caudate nucleus at the level of the foramen of Monro

56
Q

What are the 3 major etiologic sydnromes of CP?

A
  1. matrix hemorrhages in the immature infant
  2. HIE
  3. Other developmental motor abnormalities like intrauterine stroke
57
Q

What proportion of subependymal hge patients will have periventricular leukomalacia?

A

1/3

58
Q

What is the rate of mortality and neurodev disability for HIE bebes?

A

Neurodev 25%

Mortality 20%

59
Q

What is the most commmon neuroimaging correlate for CP in the european cerebral palsy study?

A

Periventricular leukomalacia

60
Q

What type of HIE? Fenichel et al.

  1. hyperaltertness and jittery baby first 24 hours
  2. EEG is normal
  3. irreg respirations needing MV at birth
  4. EEG is abnormal may improve from obtunded after 48 hours or may worsen
  5. Hypotonic limbs, no moro, depressed sucking and swallowing
A
  1. hyperaltertness and jittery baby first 24 hours 1
  2. EEG is normal 1
  3. irreg respirations needing MV at birth 3
  4. EEG is abnormal may improve from obtunded after 48 hours or may worsen 2
  5. Hypotonic limbs, no moro, depressed sucking and swallowing 3

Type 1 mild: Jittery baby in the first 24 hours. Normal tone except for head lag during traction. NORMAL EEG
Type 2 moderate: Obtunded hypotonic. post 72 hours may get better or worsen. EEG is abnormal.
Type 3 severe. Stupor and coma at birth. Hypotonic and motionless. Requiring MV. Abnormal EEG.

61
Q

What is the classic position of the LE in spastic diplegia?

A

Scissors

62
Q

What does the presence of statu marmoratus (etat marbre) say about the timing of a cerebral lesion? Seen in the basal ganglia and thalamus in patients with young patients with extrapyramidal syndromes

A

That the insult occurred BEFORE infancy before myelination has completed its early developmental cycle

63
Q

Serum bilirubin level greater than ____ mg dl when kernicterus develops.

A

25

64
Q

What should be suspected if extrapyramidal syndrome is accompanied by bilateral deafness and paralysis of upward gaze? Lesions in the GP, Thalamus, STN, CN3 and CN8

A

Kernicterus

65
Q

What is the Crigler Najjar syndrome?

A

Hereditary hyperbilirubinemia due to deficiency in glucoronosyltransferase

66
Q

What part of the cerebellum is missing in Jourbert syndrome?

A

Dysgenisis of the vermis causing the molar tooth sign on MRI

67
Q

What tumor causes opsoclonus myoclonus ataxia?

A

Neuroblastoma

68
Q

What two TORCH infections have calcifications?

A

Toxo (widely disseminated) and CMV (periventricular distribution)

69
Q

What two TORCH infections cause deafness?

A

Rubella and CMV

Neurosyphillis also causes deafness

70
Q

What is the tetrad of rubella congenital?

A

Cataracts
Deafness MOST COMMONW
Congenital heart disease
Developmental delay

71
Q

What is the treatment for active infection of CMV and congenital rubella in then newborn?

What about toxoplasmosis?

A

None

Pyrimethamine and sulfadiazine

72
Q

What are the eye lesions in toxoplasmosis?

A

Chorioretinitis

73
Q

What is the Hutchinson triad of syphillis?

A

Keratitis
Dental deformity
Bilateral deafness

74
Q

What age group do these epileptic states occur in:

  1. Febrile seizures
  2. Generalized temporal spike wave activity with benign motor and complex partial seizures
  3. Petit mal seizures
  4. Myoclonic or extensor spasms
A
  1. Febrile seizures 6 months to 6 years
  2. Generalized temporal spike wave activity with benign motor and complex partial seizures 6 years to 16 years
  3. Petit mal seizures 4-13
  4. Mid to late adolescent years
75
Q

What may be the only physicla abnormality in Fragile X?

A

large testes

76
Q

What is the cut off IQ for developmental delay that allows for independent living?

A

60 and up

77
Q

What are the to somatic hallmarks of Prader Willi syndrome?

A

Obesity and hypogenitalism

78
Q

What characteristics rhythmias or movement stereotypies are characteristic of the following syndromes?

  1. Autism:
  2. Rett syndrome:
  3. Down syndrome:
A
  1. Autism: hand flapping
  2. Rett syndrome: hand wringing
  3. Down syndrome: hand waving
79
Q

What is the repeated unstable sequence in Fragile X syndrome that leads to breakage at the distal end of the long arm of X chromosome? How do the testes look?

A

CGG
Large testes

Remember the disease affects males mostly

80
Q

Fragile premutation syndrome in adults can be described as?

A

Adult onset ataxia, tremor, midl retardation and autistic like behavior

81
Q

What is the genetic basis for rett syndrome and why is it only seen in girls?

A

Defect at the chromosomal Xq28 gene MECP2– fatal outcome in boys and mosaic condition in girls

82
Q

What are three characteristic features of Williams syndrome?

A
  1. Striking sociability and empathy
  2. Supravalvular aortic stenosis
  3. Memory for musical scores

Think Prince William! WIlliamStenosis

83
Q

What is the eponym for autism? Asocial, lacking in communicative skills in both verbal and non verbal and committed to repetitive ritualistic behaviours

A

Kanner Asperger syndrome

84
Q

What percentage of autistic patients have an IQ that is normal or superior?

A

1%

85
Q

What are the 4 core elements of autism?

A

Social
Language
Cognitive
Behavioural

86
Q

What are the serotonin levels in autism?

A

Increased in platelet but decreased in serum– SSRIs can be used for mood swings

Brain Power: Adam and Victor's Neurology (19 decks)

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