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MT1 Cases and presentations Flashcards

1
Q

what is spina bifida?

A

neural tube is not compeltely closed

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2
Q

what is the cause of SB?

A

unknown cause

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3
Q

what are the types of SB?

A

occulata
meningocele
myelomeningocele

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4
Q

what are risk factors associtated with SB

A 
o	Folate deficiency during pregnancy
o	Family history 
o	Obesity
o	Medications; anti-seizure
o	Diabetes
o	Elevated body temperature
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5
Q

what are some signs and symptoms associated with SB?

A

in myelomeningocele: weakness of limbs, loss of sensation, foot malformation, siezures, bowel/bladder dysfuntion

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6
Q

treatments for SB?

A

surgery pre or post birth

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7
Q

detection of SB?

A

SB occulata can only be detected after birth

the two other types can be detected via blood test and ultrasound

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8
Q

role of PTOT with SB?

A

o Help address muscle weakness
o Provide independence in ADLs
o Assistive technologies
o Patient mobility

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9
Q

SB on psychosocial aspect

A
  • socialization
  • attention deficit
  • limited accessibility
  • difficulty accomplishing ADLs
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10
Q

What is DMD?

A

X-lined recessive disease that causes a mutation in dystrophine

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11
Q

who is more at risk of DMD

A

males,

females are crriers

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12
Q

what % of people are affected by DMD?

A

1/3500 WORLDWIDE

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13
Q

What are some signs and symptoms associated witn DMD

A

toe walk and glute max gait
lack of stability
loss of motor functions
disruption of brain finctions

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14
Q

diagnosing DMD?

A

genetic tests
muscular biospies
CK testing

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15
Q

what are some disabilites associated with DMD?

A

Cognitive
cardiac/cardiomyopathy
scoliosis
difficulty breaking (death is often caused by this)

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16
Q

psychosocial aspects of DMD

A

limited participation
transport limitations
self esteem

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17
Q

treatment for DMD

A

NO CURE

corticosteroids to reduce muscle weakness

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18
Q

PTOT involvement in DMD

A

 Maintain ambulation and independence as long as possible
 Improve rom
 Reduce loss of strength
 Stretching to prevent contractions and muscle imbalances
 Assistive technologies

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19
Q

What is MS

A

o Neurodegenerative autoimmune inflammatory that affects the CNS

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20
Q

what happens to the myelin sheaths in MS patients?

A

damage which slows down signal transmission

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21
Q

how is MS classified?

A

based on relapses, disease progression and lesion development

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22
Q

what are the different types of MS

A

primary progressive MS
secondary progressive MS
primary progressive relapsing MS
relapsing remitting MS

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23
Q

what causes MS?

A

unknown

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24
Q

what are some risk factors associated to MS?

A

o Children of parents with MS are more at risk

o Viral infections (epinstein barr) low vit D and type 1 diabetes have been linked to MS

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25
who is more affected by MS?
females ~32 years old smokers northern eastern europeens
26
what are some signs and symptoms associated with MS?
``` Numbness/tingling pain weakness visual disturbances fatigue spasticity ataxia bladder/bowel and sexual dysfunction loss of balance difficulty speaking or swallowing ```
27
how can MS be diagnoes?
analysis of reoccurance os symptoms; must last 24H and be separated fromast attack for over 1 month MRI, Lumbar puncture, evoked potentials
28
what are some psychosocla aspects associated with MS?
loss of independence overwhelming symptoms limited social interactions emotional incomfort; burden, self-esteem etc
29
possible treatments for MS?
no cure | can use medication as muscle relaxants, corticosteroid, disease modifying drugs
30
implications of PTOT with MS?
 Stretching and strengthening to reduce muscle weakness and spasticity  Energy conservation techniques
31
hydrocephalus?
o Buildup of CSF in the CNS due to blockage of flow, impeded absorption of CSF or excessive CSF production o Accumulation results in enlargements of the brain ventricles and increases ICP
32
what are the different types of hydrocephalus?
acquired or congenital
33
what population groups are more prone to developing hydrocephalus?
infants and older adults
34
who is more at risk of NPH?
MALES | >60 YO
35
what are some possible causes of hydrocephalus?
congenital disorders such as spina bifida, complications during premature birth, tumors in the CNS, infections (meningitis) or hemorrhage
36
how can hydrocephalus be detected?
MRI/CT scans
37
what are some signs and symptoms in infant hydrocephalus?
``` skull expansion irritability down deviation vomiting sleepiness occular impairments personality changes bladder incontinence ```
38
symptoms of hydrocephalus can be confused with what other illnesses?
 Alzheimer  Parkinson’s  Creutzfeldt-jakob
39
psychosocial aspects of hydrocephalus?
- decreased cognition and devlopment in children - limited ADLs - difficulty interacting
40
treatments for hydrocephalus
surgical shunt system | third ventriculostomy
41
implication of PTOT in hydrocephalus?
address permanent impairments and help follow developmental model
42
what causes TSCI?
external impact
43
what are the main causes of TSCI?
Falls, MVA, Sports, assults
44
who is more at risk of TSCI?
men/ teens adults for MVA | >70 yo for falls
45
signs and symptoms of TSCI?
``` o Back pain and neck pressure o Weakness/paralysis o Numbness/tingling or sensory loss o Bladder/bowel dysfunction o Impaired breathing o In acute phase; Spinal shock ```
46
diagnosis of TSCI?
o Imaging techniques o Lab studies of arterial blood gas, lactase levels, Hb or Ht levels o Urinalysis will provide more info about the extent of the injury
47
Psychosocial aspects of TSCI?
``` limited transportation and accessibility loss of autonomu negative emotions secreased sociability high rate of unemplyments ```
48
treatment for TSCI?
- acute center to rehab center - immobilize neck and SC - surgery in the case of compression - medication for pain and spasticity - methydprednisolone can improve motor function
49
role of PTOT in TSCI?
o PT/OT: muscle strengthening, fine motor skills, education, adaptive ADLs o Technologies including robotic gait training
50
Risk factors of stoke?
```  Heart disease  CAD  Hypercholesterolemia  Hypertension  Diabetes ```
51
consequences associated to stokes?
location of lesion willimpact functions
52
left lesion in stoke patients?
right hemiparesis of face and UE contralateral sensory loss gaze preference to the lefr
53
infarct on dominant side
expressive aphasia
54
infarct on non dominant side
disturbance of spatial awareness
55
treatments for stoke
IVT to unblock clot from vessel (4-5H after stoke) mechanical thombectomy (24H after symptoms) decrease of ICP using clipping, burr ghole or endovascular therapy medication such as balcofene
56
involvement of PTOT in stroke patients?
teach adaptive techniques and help them in accomplishing ADLs as independently. Use FES to improves motor skills or use of CIMT which forces patient to use weaker limb and break the non-use pattern established
57
psychosocial aspects in stoke patients
``` loss of speech, continues to understand weakened muscles of the mouth UMN lesions limited social network pain decreased ADLs ```
58
what is BPA?
 Complete lesion of some or all C5-T1 preganglionic or post ganglionic spinal nerve roots from the SC
59
what causes BPA
MVA, high contact sports, birth complications, tumors etc
60
in what position do lesion in the BPA occur?
falls on the neck and shoulder which are stretch inferiorly and laterally
61
what population is most at risk of BPA?
men ages 21-30 are most at risk due to MVA
62
what are some signs and symptoms associated with MVA
sensory impairements muscle weakess total or partial losses
63
diagnosis of BPA
Physical signs; dermatomes and myotomes imaging techniques; ct 3-4 Weeks after, MRI to asses damage EMG to determine motor functions
64
impairments associated with bPA
``` chronic pain stiff joints muscle atrophy numbness erbs palsy klumpe palsy ```
65
psychosocial aspects of BPA?
- adl modification - transport - emotional - limited participation
66
treatments for BPA
surgeries to restor motor/sensory function nerve remplacements muscle and tendon transfers to athrophies muscles wear brace during recovery medication to relieve pain
67
involvement of PTOT in BPA?
 Rehabilitation: stretching and exercises to amplify UL ROM, joint flexibility & work on ADLs and fine motor skills
68
how can stroke be prevented?
diet modifications PA smoking
69
why is smoking a risk factor associated to stoke?
fatty buildup and nictoine increases BOP
70
ALS?
o Neurological diseases that targets a-MN for voluntary movements
71
cause of ALS?
UNKNOWN
72
what may contribute to ALS?
``` glutamate excitotoxicity increased intracellular Ca2+ abnormal macrophage activity in CSF Toxins genetic mutations physical trauma ```
73
what population is most at risk of ALS due to intense PA?
veterans
74
ALS in more common in who/
men ~40-60 Y/o
75
signs and symptoms of ALS
```  Progressive muscle weakness  Shortness of breathe  Decreased muscle tone  Spasticity  Difficulty walking  Lack of motor coordination  Increase or decrease in reflexes  Dysphagia  malnutrition  Respiratory failure that will eventually cause death ```
76
how to diagnose ALS?
Series of test to rule out MS and primary lateral sclerosis | blood work, biopsises, urine tests
77
psychosocial aspects ALS
``` o Loss of independence o Inability to speak, swallow, breathe o Restricted o Limited ADLs o Limited ambulation o Feels helpless, confined, fatigued, depressed ```
78
treatments ALS
no cure | medication to slow down MN degradation or to decline clinical assessment
79
involvement of PTOT in ALS?
 Facilitate movements with equipment |  Muscle stretching, resistance and functional training
80
What are some increased risks associated with NTSCI?
o Increased risked if you have arthritis, osteoporosis, disk prolapse or degeneration, tumors, epidural abscesses
81
Who is most at risk of NTSCI?
o Greater prevalence in men between 75-84 years old.
82
what is the incidence of NTSCI per year
68M
83
what are some signs and symptoms of NTSCI
Loss of sensory and motor functions bladder/bowel/sexual dysfunction spasticity pain
84
diagnosis NTSCI
patient history imagery neurological testing
85
psychosocial aspects of NTSCI?
Loss of independence mobility and transport limitations burden
86
treatment for NTSCI?
Surgery in cases or tumors, hematoma or degenrative SC conditions to prevent further damage medication to alleviate paIn
87
involvement of PTOT in NTSCI
improve fine motor skill, stretch muscles, teach new techniques to ease ADLs. o Adaptive technologies to promote independence

POTH 455 (6 decks)

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