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PPC2 Exam 3 > Neuro 1 > Flashcards

Neuro 1 Flashcards

1
Q

Plain Radiograph of skull (3)

A
  1. Linear fracture
  2. Craniosynostosis
    * Birth defect in which one or more of the fibrous joints between the bones of your baby’s skull (cranial sutures) close prematurely (fuse)
    * Skull X-ray is first line test
    * Less radiation than a CT with bone windows
  3. Ordered if a baby came in and hit their head and you’re considering a skull fracture
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2
Q

Cranial ultrasound in infants and neonatal period (7)

A
  1. Examines size of ventricles, subdural effusions
  2. Will rule out enlarged ventricles as source of macrocephaly.
  3. Used to monitor intraventricular hemorrhage in nursery
  4. Use this if someone has an open fontanel
  5. Good way to examine the ventricles and subdural effusions
  6. Non-invasive and safe, done without sedation
    * Very good sensitivity and specificity
  7. If someone has an enlarging head circumference → first line test is ultrasound
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3
Q

Ultrasound of sacral spine (5)

A
  1. Done prior to three months when the ossification of the posterior vertebral elements occur
  2. If someone has a dimple at the base of their spine, hair tufts over spine or erythematous or nevous flameus over dimple
  3. Use ultrasound of sacral spine to rule out spina bifida occulta
    * Can be picked up before 4 months old without having to put the child in an MRI
    * If ultrasound is positive, order MRI of LS spine to look for spina bifida
  4. Can evaluate spinal anomalies, vertebral defects, and cord motion
  5. Will pick up a tethered cord
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4
Q

Computerized tomography (CT) of head (8)

A
  1. Trauma
    * Send to CT because it is very quick – use if a child has been in an accident, etc.
  2. Craniofacial
    * Bone windows
  3. Temporal bone disease
  4. Size of ventricle
  5. Bony changes of histiocytosis, neuroblastoma
  6. Does not image posterior fossa, brain stem as well as MRI
  7. Involves a lot of radiation
  8. Images blood well in the emergency room
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5
Q

Radiation Risk and CT Scanning (5)

A
  1. Children at greater risk
  2. Inherently more radiosensitive and they have more life years to get radiation induced cancer
  3. CT of head and abdomen: most common
  4. Looked at radiation exposure, younger the child the more dangerous it is
    * The younger the child, the more radiation
  5. Can increase cancer risk
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6
Q

MRI (5)

A
  1. Can detect intrinsic changes in water content and soft tissue of the brain.
  2. Can give image with high spatial resolution as well as multiple planes and three dimensional images
  3. Good for imaging posterior fossa and brain stem.
    * Requires sedation
  4. Open MRI images are not as good as closed MRI
    * Constrast dye
  5. NEED to get normal renal functions before MRI
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7
Q

Functional MRI (3)

A
  1. Used to measure minutes changes in cerebral blood flow during visual, motor or verbal tasks.
  2. Can be useful for mapping cortical speech and motor area prior to resection of brain tumors or seizure foci
  3. Uses dye
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8
Q

Magnetic Resonance Spectroscopy (3)

A
  1. Helpful in evaluation of brain chemistry
  2. Helpful in determining degree of malignancy of brain tumor and metabolic abnormalities
  3. Used a lot in neuro oncology, primary care not ordered with MRS
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9
Q

Magnetic Resonance Angiography (4)

A
  1. Imaging blood flow in the large arteries and veins
  2. Can evaluate vessel patency, flow magnitude, as well as flow direction
  3. Images intracranial vasculature without use of angiography.
  4. Good for aneurysms, vascular malformations, arterial trauma, and occlusive vascular disease
    i. Vascular anomalies of the brain
    ii. Bleed in brain, aneurysm, or some moya-moya disease, or arterial disease
    iii. MRA = vascular blood vessel abnormalities
    iv. Kids with sickle cell*
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10
Q

Myotonic Muscular Dystrophy: MMD1 (6)

A
  1. Most common type of MMD seen in children
  2. Results from an abnormal DNA expansion in the DMPK gene on chromosome 19.
  3. The age of onset is roughly correlated with the size of the DNA expansion
  4. Caused by abnormally expanded stretches of DNA.
  5. The expansions effect various cells, particularly the cells of the voluntary and involuntary muscles, including the heart and some nerve cells
  6. Inherited in an autosomal dominant pattern
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11
Q

Congenital-onset MMD1 (5)

A
  1. Begins at or around the time of birth
  2. Characterized by severe muscle weakness, cognitive impairment and other developmental abnormalities.
  3. Occur only when the DMPK gene flaw comes from the mother.
  4. A mother with a small CTG repeat expansion and few or no noticeable symptoms can give birth to a baby with a large CTG expansion and the congenital- onset form of MMD1.
  5. Repeats lead to cognitive impairments
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12
Q

Juvenile-onset MMD1 (4)

A
  1. Begins during childhood (after birth but before adolescence)

Characterized by

  1. Cognitive and behavioral symptoms
  2. Muscle weakness
  3. Myotonia (difficulty relaxing muscles after use) and other symptoms → difficulty letting go of hand
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13
Q

Adult-onset MMD1 (6)

A
  1. Begins in adolescence or early adulthood

Characterized by

  1. Slowly progressive weakness
  2. Myotonia
  3. Cardiac abnormalities
    * Arrhythmia and can kill them
  4. Kids also get seen by cardiology
  5. Sometimes, mild to moderate cognitive difficulties
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14
Q

Medical Management of MMD1 (9)

A
  1. No Cure – Currently enrolling for clinical trials
  2. Vision Screening- cataracts and strabismus: common
  3. Cardiac Disease- Cardiomyopathy and arrhythmias
  4. Anesthesia concerns- high risk for complications
  5. Respiratory- BiPAP may be required, annual pulmonary evaluations
  6. Cognitive and behavioral abnormalities -
    Neuropsychiatric evaluations
  7. Difficulty chewing and swallowing- GT may be needed; choke, cannot swallow
  8. Insulin resistance- Diabetes may evolve, close monitor and management
  9. Muscle Weakness and Pain- Scoliosis management, adaptive equipment as needed
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15
Q

Myasthenia Gravis Overview

A
  1. Autoimmune disease

2. Antibodies are directed against the postsynaptic membrane of the neuromuscular junction

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16
Q

Myasthenia Gravis Clinical Manifestations

A
  1. Muscle weakness including difficulty swallowing fatigability
  2. Prepubertal children - higher prevalence of isolated ocular symptoms
  3. Lower frequency of acetylcholine receptor antibodies
  4. Higher probability of achieving remission
    * Weaker at the end of the day rather than the beginning = think myasthenia gravis
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17
Q

Myasthenia Gravis Diagnosis (5)

A
  1. PE consistent with MG (Ptosis, diplopia, ect.)
  2. Serologic testing for ACH binding, blocking, modulating, and antiMUSK antibodies
  3. If the blood tests are negative-electrodiagnostic testing
    * In MG, a muscle’s response to repeated nerve stimulation declines rapidly.
  4. Tensilon test: a fast-acting cholinesterase inhibitor.
    * A temporary increase in strength after this “Tensilon test” is consistent with MG.
    * Increase in strength
  5. If a diagnosis of MG is confirmed, a CT scan, or magnetic resonance imaging (MRI) of thymus
    * Look for thymoma = reason in a young kid
18
Q

Myasthenia Gravis Treatment Options (4)

A
  1. Acetylcholinesterase inhibitors (first line)
  2. Thymectomy (post pubertal children usually)
  3. Steroids used in combination with steroid sparing agents such as Azathioprine, Cyclosporine A, Cyclophosphamide, Tacrolimus, Rituximab
  4. IVIG, Plasmaphoresis (to remove antibodies)
19
Q

Myasthenia Gravis Warnings (7)

A
  1. Many prescription drugs can unmask or worsen symptoms of MG.

These include:

  1. Muscle relaxants used during surgery
  2. Aminoglycoside and quinolone antibiotics
  3. Cardiac anti-arrhythmics
  4. Local anesthetics
  5. Magnesium salts (including milk of magnesia)
  6. Respiratory failure when given cipro*** throws into myasthenic crisis
20
Q

Myasthenic Crisis (3)

A
  1. Myasthenic crisis, an extreme episode of weakness that culminates in respiratory failure and the need for mechanical ventilation.
  2. In some cases, the respiratory muscles themselves give out, and in others, weakness in the throat muscles causes the airway to collapse.
  3. Myasthenic crisis can occur without warning, but it often has an identifiable trigger: Fever, respiratory infection, traumatic injury, stress, or drug
21
Q

Neuromuscular Diseases (6)

A
  1. In all cases of suspected neuromuscular disease refer to a Neuromuscular Center (MDA Clinic).
  2. There is at least one clinic in every state!
  3. Refer EARLY, clinical trials are ongoing and early detection and proper management can greatly improve morbidity and mortality.
  4. Include muscle disease in you differential when you see and elevated AST/ALT.
    * Muscular difficulties will have sky high AST and ALT
  5. Encourage vaccines!
    * Influenza can kill a patient with a neuromuscular disease.
  6. There is no such thing as a LAZY baby! Investigate further.
22
Q

Macrocephaly and Physical Assessment (5)

A
  1. Transilluminate head with light.
  2. Listen for cranial bruits.
  3. Look for signs of increased intracranial pressure
  4. Assess for signs of neurocutaneous disorders —café-au-lait spots, multiple epidermal nevi, and hypopigmented macules.
  5. Carefully evaluate for extraocular movement particularly upward gaze (Intracranial pressure increase).
23
Q

Macrocephaly bony abnormalities (5)

A
  1. Neurofibromatosis and café au lait go together
  2. EOM should be evaluated because maybe they have increased ICP
  3. Palsy on upward gaze
  4. Multiple epidermal nevi – can be in brain and have a big head
  5. Short extremities (Achondroplasia)
24
Q

Reasons for Megalencephaly (5)

A
  1. Megalencephaly - head circumference > 98th percentile for age and sex
  2. Anatomic: Due to increase in brain substance as a result of an increase in size and number of brain cells
  3. Genetic: Parental head circumference is large and child’s development and neurological exam is normal
  4. Associated with syndromes such as neurocutaneous disorders, achondroplasia, cerebral gigantism (Soto’s syndrome), Fragile X
  5. Metabolic: Due to the deposit of metabolic products without an increase in the number of cells (Inborn Error of Metabolism)
25
Q

External Hydrocephalus (5)

A
  1. Benign enlargement of subarachnoid space in the frontal or frontoparietal region
  2. Usually improves by 18 months
  3. Delay reabsorption of CSF by the vessels in subarachnoid space
  4. Present with macrocephaly with a full but pulsatile anterior fontanel with normal ventricles.
  5. Head size rapidly increases to 90% and then parallel the growth curve.
26
Q

External Hydrocephalus Incidence (4)

A
  1. Common in male infants
  2. Benign accumulation – causes head circumference to cross 2 lines
  3. Do an ultrasound and external hydrocephalus
  4. Actual hydrocephalus they will have large ventricles
27
Q

Microcephaly (5)

A
  1. Head size that is two standard deviations below the mean for age, gestational age, and gender.
  2. In a normal small head,
  3. Brain should appear normal in sulcal pattern and have no destructive lesions.
  4. If the head is 3 standard deviations below the mean,
    * Higher incidence of developmental delay with cognitive impairment
  5. Refer to genetics and neuro
28
Q

Primary microcephaly genetics (4)

A

GENETIC

  1. Lack of brain development
  2. Autosomal dominant form of familial microcephaly
    * Milder
  3. Associated with normal intelligence/mild mental retardation
  4. Autosomal recessive form
    * Parents have normal head is associated with more severe mental retardation
29
Q

Secondary microcephaly (3)

A
  1. Results from insult occurring to a normal brain during the last part of the third trimester, during delivery, neonatal period or in early infancy.

Prevalence

  1. 2.5% of all newborns with the severity of the microcephaly being related to the severity of mental retardation.
  2. Zika virus link
30
Q

Perinatal Factors and Microcephaly Results from? (4)

A
  1. Vascular damage to the developing brain from neonatal stroke
  2. Thrombosis of the vessel
  3. Hypoxic-ischemic encephalopathy
  4. Intracranial hemorrhage or from congenital infection.
31
Q

Perinatal Factors and Microcephaly Age of Onsets (3)

A
  1. Most common form of brain injury: Hypoxic-ischemic disease
  2. Term infant: Neuronal injury predominates
  3. Premature infant: Oligodendroglial or white matter injury predominates
    * Very low birth weight infant
    * 30 to 50% of infants are in the subnormal range in academic achievement

32
Q

Microcephaly Treatment (3)

A
  1. Make sure all members of family are functioning normally
  2. If prematurity and microcephaly
  3. Close primary care follow-up including monitoring compliance with subspecialty referrals—ophthalmology, neurology, audiology, developmental pediatrics, and early intervention
33
Q

Disorders that can Mimic Seizures (7)

A
  1. Syncope and convulsive syncope
  2. Non-epileptic seizures (psychogenic)
    * Not post-ictal as long as you expect
  3. Pain reactions
  4. Panic Symptoms
  5. Dissociative episodes and other psychiatric states
  6. Sleep disorders
  7. Narcolepsy
34
Q

Classification of Epilepsies: Seizure Type (3), Epilepsy Type (4), Epilepsy Syndrome (1)

A
  1. Seizure type
    a. Focal onset
    b. Generalized onset – grand mal
    c. Unknown onset
  2. Epilepsy type
    a. Generalized
    b. Focal
    c. Combined Generalized and focal Epilepsy
    d. Unknown
  3. Epilepsy Syndromes
    a. Because of genetics – there is a category of epilepsy syndromes
35
Q

Etiologies of Epilepsies (6)

A
  1. Etiologies
    a. Structural etiology
    b. Well known findings of mesial temporal lobe seizure with hippocampal sclerosis
    c. Gelastic seizures with hypothalamic hamartoma
  2. Genetic etiology
    a. Best known Dravet syndrome is a pathogenic variant of SCN1A
  3. Infectious etiology
    a. Neurocysticercosis, TB, HIV, Cerebra malaria or toxo, congenital zika
    b. Neurocysticercosis – grand mal seizures, traveled and lived in south america
  4. Metabolic: aminoacidopathies, pyridoxine dependent
  5. Immune: anti-NMDA receptor encephalitis
  6. Unknown etiology
36
Q

Focal Onset Seizures

A

Local or widely distributed with focal seizures originating in subcortical structure
*Focal seizure is then classified based on level of awareness during the seizure, not to whether the seizure has occurred

37
Q

Generalized Onset Seizures (5)

A
  1. Motor or nonmotor (absence seizures)
  2. Level of awareness is not used classifier for generalized seizures
  3. Do not respond
  4. After seizure, sleep more than usual
  5. Non-motor generalized seizure = can look like day dreaming, do not respond, probably from the temporal lobe
38
Q

Additional Descriptions of Seizures (4)

A
  1. Bilateral versus generalized (simultaneously in both hemispheres)
  2. Atypical absence is it has a slow onset or offset, marked change in tone or EEG at < 3 per second
  3. Clonic versus myoclonic: clonic is sustained rhythmic jerking and myoclonic to regular unsustained jerking
  4. Eye myoclonia: absence of the eyelid myclonia refers to forced upward jerking of the eyelid during an absence seizure
39
Q

Focal Motor Onset Behaviors (10)

A
  1. Atonic (focal loss of tone)
  2. Tonic (sustained focal stiffening)
  3. Clonic (focal rhythmic jerking)
  4. Myoclonic (irregular, brief, focal Jerking
  5. Epileptic spasms (focal flexion or extension of arm and flexion of trunk)
  6. Focal motor seizure with behavior arrest involves cessation of movement and unresponsiveness
  7. Focal autonomic seizures present with gastrointestinal symptoms, sense of heat or cold, flushing, piloerection, palpitation, respiratory changes or autonomic effects, sexual arousal
  8. Focal emotional seizures present with emotional changes—fear, anxiety agitation, anger, paranoia, pleasure joy, ecstasy, laughing (gelastic) or crying (dacrystic)
  9. Can produce somatosensory, olfactory, visual, auditory, gustatory, hold-cold sense or vestibular sensations
  10. Smell something, hear something, vestibular or personality can change = anger
40
Q

New Types of General Onset Seizures

A

Motor

  1. Grand mal replaced with tonic clonic i
  2. Must know initial phase of seizure—tonic or clonic
  3. Generalized myoclonic-tonic-clonic seizures begin with myotonic jerks follow by tonic clonic activity (juvenile myoclonic epilepsy
  4. Nonmotor (absence)

PPC2 Exam 3 (14 decks)

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