SLT Role Flashcards
1
Q
acute disorders of the CNS
A
- Hypoxic-ischemic encephalopathy
- Intracranial vascular events (e.g., infarction)
- Intraventricular hemorrhage (IVH)
- Infections (e.g., meningitis)
- Metabolic conditions
- Trauma
- Encephalitis
2
Q
chronic disorders of the CNS (static course)
A
- Cerebral Palsy
- Genetic disorders
- Arnold–Chiari Malformation
3
Q
chronic disorders of the CNS (progressive course)
A
- Muscular Dystrophies
- Spinal Muscular Atrophies (SMA)
- Rett Syndrome
- Intracranial malignancies
- Rasmussen Encephalitis
4
Q
chromosomal conditions
A
- Trisomy 21 (Down Syndrome)
- Cystic Fibrosis
- Sickle Cell Disease
5
Q
impact of aetiologies
A
- Premature birth: Missed embryonic development
- Life-limiting
- Delayed development (feeding, communication)
- Chronic illness & frequent hospitalizations
- Missed critical periods of development
- Skill regression or progressive loss of skills
- Co-morbidities
- Persistent primitive reflexes, abnormal reflexes
6
Q
what does feeding difficulties impact
A
physical, social, emotional and cognitive functions; increases caregiver stress
7
Q
what does paediatric dysarthria affect
A
- Communication development
- Quality of life
- Social interaction and participation
8
Q
what percentage of children with cerebral palsy have motor speech impairments
A
33-63%
9
Q
what is the proper name for a brain tumor
A
intercranial malignancy
10
Q
what are the most common solid tumours in children
A
brain and spinal tumours
11
Q
what are the most common causes of cancer deaths
A
CNS tumours
12
Q
what causes brain tumours
A
Brain tumors occur due a genetic alteration in normal brain cells, causing the cells to undergo a series of changes which result in a growing mass of abnormal cells.
13
Q
where do primary brain tumours start
A
in the brain (i.e. not spread from anywhere else)
14
Q
what does low-grade tumour mean
A
less agressive tumour
15
Q
what does high grade tumour mean
A
very agressive tumour
16
Q
causes of intracranial malignancies
A
mostly unknown, some have hereditary germ line mutations
17
Q
common types of intracranial malignancy
A
- Medulloblastoma
- Diffuse Midline Glioma (DMG)
- Atypical Teratoid Rhabdoid Tumor (ATRT)
18
Q
how many children are diagnosed with intracranial malignancy anually
A
60
19
Q
what is the most common site of intracranial malignancies
A
posterior fossa
20
Q
what percentage of childhood intracranial malignancies are in the posterior fossa
A
60%
21
Q
what causes cerebral palsy
A
early brain injury (in utero, during or after birth)
22
Q
course of cerebral palsy
A
Born with a normal musckoskeletal system at birth, bur develop postural problems over time
23
Q
incidence of cerebral palsy
A
1.4 per 1,000 live births
24
Q
what percentage of cerebral palsy cases are caused by white matter damage (PVL)
A
45%
25
is CP caused by white matter damage more common in preterm or term injuries
preterm
26
what type of CP is most commonly associated with white matter damage
spastic type
27
what percentage of CP cases are caused by basal ganglia or deep matter damage
13%
28
what type of CP is most commonly associated with basal ganglia or deep grey matter damage
dyskinetic CP
29
what percentage of CP cases are caused by congenital malformations
10%
30
are CP cases caused by congenital malformations more common in preterm or term
term
31
what percentage of CP cases are caused by focal infarcts
7%
32
what is a chiari malformation
- **Brainstem and spinal cord compression**
- Lower part of brain pushes down into spinal canal.
- Pressure is placed on the brainstem and spinal cord.
- Flow of fluid is obstructed.
33
subtypes of Chiari malformation
- chiari I
- chiari II
- chiari III
34
symptoms of chiari I
often no symptoms
35
what is chiari II associated with
Associated with neural tube defects (myelomeningocele)
36
which chiari subtype has the most sever symptoms
chiari III
37
issues assocated with chiari malformation
Hydrocephalus, saliva control, swallowing problems (cranial nerve compression).
38
two main types of encephalitis
infectious and autoimmune
39
three subtypes of infectious encephalitis
- viral
- arbovirus encephalitis
- bacterial/fungal
40
what is the most common type of infective encephalitis
viral
41
what leads to arbovirus encephalitis
flea/tick/mosquito bites
42
what is the least common type of infectious encephalitis
bacterial/fungal
43
what causes autoimmune encephalitis
immune system attacks the brain, causing inflammation affecting how the brain works
44
does infectious encephalitis have sudden or gradual onset
sudden
45
signs and symptoms of infectious encephalitis
Fatigue, headache, high fever, neck stiffness
46
does autoimmune encephalitis have a gradual or sudden onset
gradual
47
signs and symptoms of autoimmune encephalitis
Confusion, drowsiness, loss of consciousness, memory issues, nausea, personality changes, seizures, speech issues, weakness, loss of movement
48
brain growth and development in the first two years
- Cerebellum develops rapidly before birth to 1 year
- Brainstem divisions grow prenatally but slow postnatally
49
how does myelination support speech and language functions
- Myelination supports rapid neural transmission
- Important for connectivity between hemispheres and cortical/subcortical structures
- Enhances speech and language function
50
how is plasticity revelvant for language development before 1 year
- Assumes non-damaged areas of the brain are capable of assuming function.
- Left hemisphere damage **before age 1** may **shift function** to the right hemisphere
51
is hand dominance a reliable predictor of language function
no
52
two types of plasticity
structural plasticity & functional plasticity
53
structural plasticity
experiences or memories change a brain’s physical structure
54
functional plasticity
brain functions move from damaged area to undamaged areas
55
what does the WADA test do
Determines which hemisphere controls language & memory (unable to refine exact areas of function).
56
when is the WADA test useful
assisting surgical procedures.
57
WADA test procedure
Drug injected into carotid artery to temporarily disable one side of the brain and patient undergoes tests of speech, memory and motor function.
58
risks of the WADA test
Invasive, small stroke risk (0.6%-1%)
59
how does fMRI measure language dominance
Indirectly measures neuronal activity by measuring blood oxygen levels (BOLD signal)
60
when is fMRI useful
- Defines hemispheric language dominance
- Plans for surgical resection & intraoperative mapping
61
types of linguistic tasks used during the WADA test
- **Overt (spoken) tasks:** "Tell me a verb related to flower" → *"smell"*
- **Covert (silent) tasks:** Think of a verb associated with *flower*
- **Listening tasks:** Captures cortical activation for real/non-real words
62
three motor systems which control speech
- pyramidal system
- extrapyramidal system
- cerebellar system
63
pyramidal system function
Voluntary muscle control, corticobulbar tract → controls cranials nerves which innervate speech muscles
64
extrapyramidal system function
Fine-tunes movement; complex pathways connecting clusters of subcortical motor nuclei and the basal ganglia.
65
cerebellar system function
Coordination & precise control
66
potential effects of paediatric dysarthria
- Reduced intelligibility
- Limited emotional expression through speech
- Lower confidence & social participation
- Difficulty communicating with friends and family.
67
prevalence of paediatric dysarthria
unclear
68
why is the prevalence of paediatric dysarthria unclear
due to secondary association with other conditions
69
key areas to cover in SLT case history
- Pregnancy & birth history
- Developmental milestones
- Time-course:
- **Sudden: (minutes):** Likely vascular
- **Gradual**
- **(days):** Inflammation
- (over weeks/months): space-occupying lesion.
- **Episodic:** Possible epilepsy
- **Impact of age at insult and time since insult on lesion effects:**
- **Investigations:** MRI, genetic testing, metabolic screening
- **Medication history:** Consider type and timing
- **Surgical History:** previous or planned
- **MDT involvemeent**
- Airway and Respiratory history
- Other medical conditions (more complex medical presentations = more severe feeding issues
70
aspects of a communication assessment
- **Speech:** Dysarthria, apraxia, articulation
- **Oromotor function:** Cranial nerve examination
- **Language:** Receptive/expressive abilities
- **Social communication (pragmatics)**
- **Pre-verbal skills.**
- **Narrative skills.**
- **Voice**
- **Fluency**
- **AAC options** (low-tech & high-tech)
71
two types of facial palsy
peripheral & central
72
what is damaged in peripheral facial palsy
facial nerve
73
what is damaged in central facial palsy
upper motor neuron of primary motor cortex or corticobulbar fibres
74
which type of facial palsyy affects the lower face more and why
Central palsy affects lower face more as both hemisphres contribute to movement of the upper face and unaffected hemisphere can compensate
75
three examples of standardised dysarthria assessments
- Frenchay Dysarthria Assessment
- Subsections of the DEAP
- Paediatric Radbound Dysarthria Assessment
76
key areas of a FEDS assessment
- Saliva control & secretion management
- Oro-motor examination
- Oral vs. enteral feeding
- Efficiency of feeding (mealtime duration, volume intake)
- Child’s developmental age
- Oral phase
- Oropharyngeal phase
- Airway protection
77
what is examined in an oro-motor assessment
| FEDS ax
symmetry; rate & range of movement; strength; functional, movement in actual feeding / EDS; cough
78
what is investigated in the oral phase of a FEDS ax
Sucking pattern, latch on teat/nipple, formation and control of the bolus, chewing, biting, anterior spillage, oral residue
79
what is examined in the oropharyngeal phase of a FEDS ax
Suck-swallow-breathe coordination, multiple/delayed swallows, nasal regurgitation
80
what is examined in airway protection in a FEDS ax
Coughing, voice changes, increased respiratory rate, colour change, eye tearing, drop in O2 saturation, wheeze or stridor
81
examples of paeds formal feeding ax
PEDI-EAT 10, pFOIS, SOFFI
82
F words approach to ICF
Focus on Function, Family, Fitness, Fun, Friends, Future
83
three treatment options for SMA
- nusinersen
- zolgensma (gene therapy)
- risdiplam
84
comercial name for risdiplam
evrysdi
85
how is risdiplam administed
daily oral treatment
86
what aged patients are candidates for risdiplam
younger than 19
87
characteristic feeding challenges for children with SMA
- Failure to thrive
- Tongue fasciculations
- Reduced secretion clearance
- Hypotonia
- Jaw contractures
- Weak cough
- Bulbar weakness
- Hypoventilation
- Pulmonary aspiration
88
SMA feeding interventions
- Postural support
- Change in bottle flow
- Drooling management
- Education and counselling for parents re need for enteral feeding supports.
- Change to high energy formula to allow smaller volume feeds per bottle.
89
what other professionals are involved in oral hygeine (aversion) interventions
OT and specialsit paediatric dentist
90
what is rasmussen encephalitis
- **Rare condition involving long-term worsening inflammation of of one hemisphere**
- Inflammation leads to frequent seizures and progressive and permanent brain damage.
- Leads to loss of function of affected hemisphere.
- Causes worsening weakness in one side of body and cogntive decline.
91
course of rasmussen encephalitis
Children with RE frequently enter a phase of permanent,
but stable, neurological deficits after eight to 12 months.
92
treatment of rasmussen encephalitis
- Anti-epileptic drugs may be prescribed but may not entirely control seizures.
- Often neurosurgical treatments are considered in the case of uncontrolled seizures
- Surgery may halt disease progression and stabilize seizures.
- However, most individuals with RE are left with some paralysis, cognitive deficits, and problems with speech.
93
94
what type of surgical intervention is used for children with rasmussen encephalitis
functional hemispherotomy - Surgery disconnecting the cortex of one hemisphere from the other without removing it.
95
example of an intracranial malignancy associated condition that requires SLT input
- **erebellar Mutism Syndrome (CMS):**
- Sometimes called Posterior Fossa Syndrome
- **Occurs post-surgical resection of posterior fossa tumors (typically medulloblastoma)**
- **Often transient but requires SLT intervention**
96
symptoms of CMS
- Mutism or very inhibited verbal output
- May produce sounds like high-pitched crying, whining or forced laughter
- Receptive language typically grossly intact
97
onset of CMS
delayed
98
prognosis of CMS
- Prognosis for recovery from mutism is good
- Often results in dysarthria and language impairment
99
FEDS post posterior fossa surgery
- Surgery for posterior fossa tumours in children is associated with bulbar palsy and swallowing difficulties
- This risk is not well defined in the literature and issues contributing to dysphagia following surgery are not fully understood.
- Swallowing difficulties, including silent aspiration, are an important complication of PFT resection.
