Neuro Exam Notes Flashcards

1
Q

Tx for ADHD

A

Stimulants:
Methylphenidate (Ritalin and Concerta)
Amphetamine (Adderall and Dexedrine)

Nonstimulants:
Atomoxetine
Clonidine

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2
Q

Side effects of anti epileptic drugs (5/6)

A

Sedation
Agitation
Headache
Rashes
Hair loss
Tremors
Swollen gums

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3
Q

Features of Trisomy 21

A

epicanthic folds on widely spaced eyes, poor tone, single transverse
(“simian”) palmar crease, sandal gap between 1st and 2nd toes, 3rd fontanelle,
associated cardiac murmur from ventricular septal defect.

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4
Q

List the manifestations of neurofibromatosis NF1 (presentation) (9)

A

Cafe-au-lait spots
Axillary freckling and in groin area
Neurofibromas
Lisch nodules (small nodules in iris of eye)
Optic Glioma (tumour in optic nerve)
Bone deformities (scoliosis or bowed lower leg)
Learning difficulties
Larger than average head
Short statue

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5
Q

Differentiate between NF1 and NF2

A

NF1 tumours develop anywhere in the nervous system including brain, spinal cord and nerves, dx early in childhood by age 10
NF2 is less common, tumours develop in nerves that carry sound and balance from inner ear to brain, in both ears (acoustic neuromas) resulting in hearing loss also called vestibular Schwannoma.

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6
Q

Manifestations of NF2 (4)

A

Gradual hearing loss
Ringing in both ears
Poor balance
Headaches

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7
Q

What is Schwannomatosis

A

Rare type of Neurofibromatosis
Affects people after 20. (25-35)
Tumours develop in cranial, spinal and peripheral nerves. Rarely affects nerve carrying sound and balance, don’t affect both ears like NF2.

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8
Q

Symptoms of Schwannomatosis

A

Chronic pain
Numbness or weakness in various parts of the body
Loss of muscle

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9
Q

What can cause delay in closure of fontanelle

A

Normal variation
Hydrocele
Hypothyroidism
Bone disorders
AVM

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10
Q

Causes of meningism

A

Meningitis
Encephalitis
Acute OM
Severe tonsillitis
Pneumonia
Cervical lymphadenitis

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11
Q

How would palsies in CN 3 (oculomotor), 4 (Trochlear), and 6 (Abducens) be apparent

A

III- ptosis and mydriasis down and out
IV- inability to adduct with downwards gaze there may be a head tilt
VI- inability to abduct eye

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12
Q

What conditions cause Developmental regression in paeds

A

HIV encephalopathy
Subacute Sclerosing Panencephalitis
Inherited metabolic disease involving brain
Infections and tumours

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13
Q

Types of acute recurrent headache

A
  1. Migraine
    -Throbbing
    -Unilateral
    -Aura present
    -Relieved by sleep
    -Ass/ nausea and vomiting
    -Family hx

Common in childhood, characterised by episodic, periodic paroxysmal attacks of vasoconstriction and vasodilatation of cerebral vessels following waves of cortical depolarisation

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14
Q

Causes of chronic progressive headaches

A

Raised ICP
Traction headaches
Brain tumours
Space occupying lesions
Benign raised intracranial pressure

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15
Q

Causes of chronic non progressive headaches

A

Tension headache
Psychogenic headache
Medication overuse

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16
Q

Triggers or precipitating factors for migraines

A

Anxiety
Stress
Fatigue-lack of sleep
Head trauma
Exercise
Menstruation
Diet (tyrannies containing food-release serotonin, ice cream, red wine, cheese)
Medication- contraceptive

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17
Q

Dose of paracetamol in paeds

A

15-20mg/kg/dose

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18
Q

Prophylactic meds for headaches in paeds

A
  1. Sodium channel blockers (sodium valproate)
  2. Beta-blockers -Propanolon (don’t use in asthmatics)

Use in severe cases, most children won’t need this

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19
Q

What areas of the brain maintain consciousness (awareness of self and environment)

A
  1. Ascending Reticular Activating System (ARAS) in brain stem (maintains aroused state)
  2. Cerebral hemispheres (controls contents of consciousness)
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20
Q

causes of acute non-recurrent headaches

A

Infection and fever
Toxins
Post convulsions
Anaemia
Electrolyte imbalance
HPT
Post LP
Hunger
Trauma

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21
Q

What causes acute and recurrent headaches

A

Migraines

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22
Q

Management of comatose patients

A

8 Principles

1.Maintain oxygenation
2. Maintain circulation
3. Control glucose
4. Lower ICP
5. Stop seizures
6. Treat infections
7. Restore acid base balance and electrolytes
8. Adjust body temperature.

(jUst think A,B,C then Hs and Ts applicable here)

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23
Q

What are the features of an organic brain lesion

A

Severe headache of recent onsert
chronic or progressive
localised pain
Wakes the child up at night
Exacerbated by straining or change in position
Associated with neurological symptoms and signs
Change in headache pattern or severity

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24
Q

dIfferentiate between a communicating and a non-communicating hydrocele

A

Communicating is due to failure to reabsorb CSF
-Subarachnoid haemorrhage
-Meningitis (e.g. TB, Pneumococcal)

Non-communicating is due to obstruction in the ventricular system
-Congenital malformation
1. Aqueduct stenosis
2. Atresia of the outflow of the foramina of the 4th ventricle
3. Chiari malformation
- Posterior fossa neoplasm or vascular malformation
-Intraventricular haemorrhage in a preterm infant

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25
Q

How do you manage raised ICP

A

EVD- External Ventricular Drainage or Shunt

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26
Q

Define epilepsy

A

2 or more unprovoked epileptic seizures more than 24 hours

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27
Q

what is status epilepticus

A

Epileptic seizures that last more than 5min or more than 2 discrete seizures with incomplete recovery of conciousness in between

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28
Q

Outline the aetiology of epilepsy

A

Structural
Infections
Genetics
Metabolic
Immune
Unknown

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29
Q

Causes of neonatal seizures

A

HIE
Intracranial haemorrhage
Cerebral infarct
Metabolic causes (hypoglycemia)
Infections
Drug withdrawal eg heroin
cortical dysplasia and malformations

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30
Q

RIsk factors for epilepsy following febrile seizures

A

Complex febrile seizures
Afebrile seizures in a 1st degree relative
Abnormal neurological signs prior to the febrile seizures

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31
Q

Management of febrile seizures

A

Antiepileptics (decrease core temp)
Antiseizure not indicated for febrile seizures
FIrst aid advise
Recue medicine for seizure lasting more than 5min
EEG nor indicated
LP to exclude meningitis in less than 18months
Neuroimaging in complex febrile seizures

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32
Q

What is West’s syndrome and what is the classical triad of West’s syndrome

A

infantile spasms syndrome was also called West syndrome. Infantile spasms syndrome is considered an epileptic encephalopathy, conditions in which children have both seizures and cognitive and developmental impairments

  1. Epileptic spasms (extensors or flexors
  2. Hypsarrhythmia on interictal EEG
  3. Cognitive and developmental regression
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33
Q

Treatment of West’s syndrome

A

Hormonal
-0ACTH
-Prednisone

Vigabatrin

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34
Q

Tx for childhood absence seizures

A

Firts line tx is Ethosuximide, Valproate, lamatrogine (less effective but side effects)

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35
Q

What is the prefered drug of choice in childbearing age women for epilepsy

A

Lamatrigine

36
Q

WHat are the causes of hypotonia (floppy child)

A

Lower Motor Neuron lesions
-Anterior horn cells (spinal cord)
1. Spinal muscular dystrophy (Hereditary)
2. Poliomyelitis (Acquired)
-Nerve Roots
3. Gullian Barre Syndrome
-Peripheral nerves
4. Demyelinating e.g Infectious polyneuritis, Peroneal muscular atrophy, Leucodystrophies
5. Diabetes, Porphyria (Axonal)
6. Hereditary motor sensory neuropathy
-Myoneural junction
7. Myasthenia gravis
Muscle
8. Congenital myopathy
9. Muscular dystrophy
10. Metabolic myopathoies
11. Myotonic syndromes

Central or Generalised conditions
1. Cerebella disorders
2. Birth trauma
3. Hypotonic CP
-Chromosomal
4. Down syndrome
5. Prada Willi syndrome
6. MArfan syndrome
7. Ehlers danlos syndrome
-Metabolic disorders
8. Hypercalcemia
9. Rickets
10. Hypothyroidism
11. Renal Tubular Acidosis
12. Coeliac disease

37
Q

Clinical features of spinal muscular atrophy (SMA)

A

Proximal muscle weakness and wasting
Facial weakness in 50%
Tongue fasciculations
Absent or reduced tendon reflexes
Sweating in soles and palms

(just think LMN lesion presentation)

38
Q

Differentiate between the different types of Spinal Muscular Atrophies (SMA)

A

Type 1:
-Presents in first few weeks of life
-Generalised Hypotonia
-Marked weakness and wasting of trunk, neck and limbs, legs more than arms
-Bulbar weakness with difficulty sucking, swallowing and cough and cry weak
-Intercoastal muscle weakness, with difficulty breathing and bell-shaped chest. Infants prone to Pneumonias
-Tendon reflexes absent
-Contractures
-Internal rotation of arms and hands with hands facing outwards

Type 2
-First few months of life
-Slower and less progressive, clin features not as severe as in Type 1
-Involvement of Resp system
-Tendon reflexes reduced rather than absent
-Tongue fasciculations

Type 3
-Usually have normal milestones in the first year but may not be able to walk

39
Q

which gene is associated with Spinal muscular atrophy (SMA)

A

It’s an Autosomal Recessive inherited condition
Gene for SMA is located on Chromosome 5

40
Q

Which organisms are associated with Guillain Barre syndrome

A

Viruses: Coxsackie, Echo virus, HSV
Campylo Jejuni
Epstein barr virus

41
Q

Causes of peripheral neuropathy in children

A

Drugs (Isoniazide, Vincristine)
Toxins (lead, mercury, gold, benzene, glue)
Hereditary motor and sensory neuropathy
Chronic inflammatory demyelinating polyradiculopathy
Metabolic neuropathies
Diabetes
Vitamin deficiencies
Krabbe disease

42
Q

Tx of Myesthenia gravis

A

Neostigmine or Pyridostigmine

Avoid aminoglycosides antibiotics, worsen it

43
Q

Treatment of hypersalivation

A

Atropine
(anticholinergics)

44
Q

What is the most common muscular dystrophy in children

A

Duchenne’s muscular dystrophy (DMD)
-Progressive weakness of proximal muscles due to deficiency of the subsarcolemmal membrane protein DYSTROPHIN
-X-linked

45
Q

Features of Duchenne’s dystrophy

A

Frequent falls
Abnormal gait
Difficulty climbing stairs
Delayed motor milestones
Toe walk

46
Q

What is Gowers sign

A

-Seen in Muscular dystrophies: Duchenne’s muscular dystrophy
-Child goes from supine to prone position, then a knee elbow position, then extending knees and elbows and slowly climb with legs supporting

47
Q

Tx of DMD (Duchenne’s Muscular Dystrophy

A
  1. Physiotherapy
  2. Glucocorticoids- steroid tx improve power, muscle mass, rate of muscle breakdown
48
Q

WHat are the 4 Types of hyperkinetic movement disorders seen in children

A

Chorea
Myoclonus
Tics
Tremors

49
Q

What is chorea, what are its causes and clinical features

A

Type of movement disorder

Clinical Presentations
-Figgety, twist or jerking in arms, legs or muscles of the face
-Grip changes (milkmaid’s grip)
-Tingue movements
-Headaches
-Seizures
-Slurred speech

(worsens when stressed, anxious, another medical condition or medication side effects)

CAuses:
1. Overactivity of Dopamine that affects basal ganglia (movement)
1. Sydenham Chorea
2. CP
3. Huntington’s
4. Endocrine: hyperthyroidism
5. SLE
6.Brain tumor in basal ganglia
7. Drug induced: Phenytoin, Lithium, Alcohol

50
Q

Tx of chorea

A
51
Q

What are the 3 commonly seen Hypokinetic disorders in children

A

Akinetic rigid syndrome
Juvenile Parkinsonism
Progressive pallidal degenerations

52
Q

List some of the most common causes of strokes in children

A
  1. Congenital heart disease
  2. Acquired heart diseases (RHD, Kawasaki, cardiomyopathy, Myocarditis, prostatic valves)
  3. HPT
  4. Atherosclerosis
  5. DM
  6. Vasculitis: Meningitis, SLE
  7. Vasculopathy: Moyamoya syndrome, HIV vasculopathy
  8. aneurysms
  9. Trauma: carotid dissection, penetrating trauma
53
Q

Which conditions are commonly linked to Moyamoya disease

A

Neurofibromatosis
TB
Sickle cell
HIV
Down Syndrome
Cranial irradiation

54
Q

What is CP

A

Group of disorders that affect movement and posture.

55
Q

Outline the causes of Cerebral Palsy

A

Prenatal
-Multiparous/Multigestation
-genetic actors
-Antenatal bleeding
-infections
-cerebral malformations
-strokes in mom ?

Perinatal
-Multiple pregnancy
-Premature
-IGR
-Small for GA
-Infections
-Birth trauma
-Perinatal strokes
-Cerebral hamerrhages

Postnatal
-Infections (meningitis)
-Head injury
-Metabolic
-hypoglycemia
-hypocalcemia
-hyponatremia
-vascular
-strokes
-thrombosis/ embolism
-toxins

56
Q

Differences between paraplegia and diplegia

A

Paraplegia (paralysis of the legs) results form a spinal cord lesion and diplegia (symmetrical paralysis of either the arms or the legs) comes from a CNS nervous system lesion

57
Q

What are the early warning signs of CP

A

Delayed milestones
Primitive reflexes or persistence of certain postures
Hypertonia or hypotonia
Clumsiness
Toe walking
Bulbar dysfunction, difficult speech, feeding and drooling

58
Q

What are the commonest causes of spastic CP (Diplegia, Hemiplegia, Quadriplegia

A

IUGR
Low birth weight
Birth asphyxia

59
Q

Differentiate between dystonia and rigidity

A

Dystonia is posture a rigid muscle is pulled into.
Rigidity is tone felt by examiner which is constant throughout range of movement

60
Q

Associatetd problems with CP/ complications

A

Intellectual impairment
Language, vision and hearing abnormalities
Epilepsy
MAlnutrition
Behavioural problems

61
Q

Common clinical features of meningitis

A

Fever
Rased ICP: vomitting, headache
Meningeal irritation: Neck stiffness, Kernigs and Brudzinski
encephalopathy and coma

In younger babies: poor feeding, irritable, bulging fontanele, vomitting and fever

62
Q

CAuses of meningitis on
1. Neonates
2. Infants
3. Childhood and adolescents

A

Neonates
-Group B strep
-Ecoli
-Listeria
-Klebsiella
-Enterobacter

Infants
-Group B strep
-Neisseria meningitis
-strep pneumonia
-Haemophilus Influenza
-Salmonella species

Childhood
-Neisseria meningitis
-Strep pneumonia
-Haemophilus Influenza

63
Q

Early sign of Neisseria meningitis

A

MEningoccoacal rash- Petechiae or purpuric rash taht can evolve very quickly into purpura fulminans

64
Q

Complications of meningitis

A

Cerebral Oedema
Hydrochephalus
Brain abscess
Seizures
Cranial mnerver palsies
Hemiolegias
Vasculitis
Subdural effusions
SISADH

65
Q

Management of Bacterial meningitis in infants less than 2 months

A

Initially:
Cefotaxime 50mg/kg 8-hourly (12 hourly if less than 1 week old)
Or
Amoicillin 50mg/kg 6-hourly (8hourly if less than 1 week old)

When organism is identified
Group B Strep: Cefotaxime or Ampicilin (alone or with aminoglycoside) for 14 days

Gram negative enteric bacilli: Cefotaxime plus aminoglycoside(1st 7 days) min 21 days

Listeria: Ampicillin alone for 14 days
Neisseria: ceftriaxone and ciprofloxacin IV? For 7days

66
Q

Tx of bacterial meningitis in infants and children older than 2 months

A

Initial therapy
Ceftriaxone 100mg/kg then 80-100mg/kg once daily OR cefoxamine 75mg/kg 8-hourly
AND
Dexamethasone 0.6mg/kg/d 8hourly ideally 15-30min priopr to initiating antibiotics

Duration of therapy
H. Influenza 7-10 days
S. Pneumonia 10-14 days
N. Meningitidis- 7days

67
Q

What prophylactic medication would you close contacts to Meningoccocal disease

A

Rifampicin
Ceftriaxone

68
Q

What prophylactic meds would you give to haemophilus influenza type B contacts

A

Rifampicin 20mg/kg daily for 4 days in 5 years and younger

69
Q

Complications of brain abscesses

A

Epilepsy
Focal neurological deficits
Hydrocephalus
Mental retardation

70
Q

Organism responsible for Neurocysticosis

A

Taenia solium the pig tape worm

Tx with albendazole or Praziquziquintel

71
Q

When should a child with spinal bifida be managed

A

refer for surgical correction within 48 hours of delivery!

72
Q

Outline the classification of seizures

A

Focal seizures:
-Aware or Unaware
-Aura
-Motor
-Autonomic

Generalised
-Tonic-clonic
-Absence
-Clonic
-Tonic
-Myoclonic

73
Q

what is a colic

A

frequent, prolonged and intense crying or fussiness in an infant, can be caused by spasm, obstruction or twisting of a gollow organ such as intestine, ureter or gall bladder

74
Q

Tx of infantile spasms (epileptic)

A

ACTH or prednisone

75
Q

Which medications do you give for Generalised Epilepsy vs
Focal Epilepsy

A

Generalised - Sodium valproate
Focal- Carbamezapine (careful in childbearing give Lamatrigine)

76
Q

Approach to Status Epilepticus

A
  • ABCD (O2, sats, pulse / BP, glucose)
  • Total 2 doses benzo….
  • Pr diazepam (0.5mg/kg) out of hospital
  • IV access IV lorazepam (0.1mg/kg) preferred

Access failure – IO line / intranasal midazolam
(200mcg/kg)
* IV phenobarbitone (20mg/kg)
* Repeat PB (10mg/kg)
* Repeat PB (10mg/kg)
* Refer PICU ……..

77
Q

Tx for migranes

A

Analgesia: Ibuprofen, Panado
Antiemetic
Migrane specific: Sumatripan (serotonin 5HT1 receptor agonist, affects vasoconstriction, oral or nasal spray tx)

Prophylaxis for migraine: Propranolol (NB in asthma, DM, CCF), Valproate (ideal in epileptics), Amitriptyline(depression), Topiramate (ideal in epileptics), Flunarizine

78
Q

Outline the 3 brainstem syndromes

A

Weber syndrome = 3rd N + opp. hemi
(midbrain)
* Millard-Gubler syndr. = 6th /7th + opp. hemi
(pons)
* Jackson syndrome = 10th, 12th + opp. Hemi
(medulla)

79
Q

differentials for hemiplegia

A

stroke
todds paralysis
ADEM
Mass lesion (neoplasisms eg)
Trauma
HSV encephalitis
COmplicated migranes
Metabolic eg MELAS

80
Q

Risk factors for stroke in children

A

Sickle cell disease
Vasculitis eg Meningitis, SLE, Takayasu
Vasculopathies e.g Post Varicella, Moyamoya
Congenital heart disease eg Complex CHD
Acquired Heart Disease eg RHD, IE
Congenital HD eg ASD ?
Genetic: NF1, Homocystinuria

81
Q

What is moyamoy and what are some of its risk factors

A

Cerebrovascular disorder, involves occlussion or stenosis or occlusion of terminal internal carotis (circle of willies?)

Risk factors
* Down’s Syndrome
* Neurofibromatosis
* Sickle Cell Disease
* Homocystinuria
* Radiotherapy (brain)
* Infections (?HIV), etc.

82
Q

What is the anatomical position of the lesion that causes cerebella motor syndrome

A

Anterior lobe of the cerebellum

83
Q

What is the location of the lesion that causes non-motor symptomatology of the cerebellum (emotion, mood, cognition)

A

Posterior lobe of the cerebellum

84
Q

WHat is the drug management and prophylaxis of sydenham chorea

A

Penicillin

85
Q

Why is Moyamoya important in SA/Africa

A

Moya moya is the endstage of vascular occlusive disease which can occur in the vasculitis associated with HIV and TB, as well as sickle cell disease, trisomy 21, and neurofibromatosis