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neuro conditions Flashcards

1
Q

What are anatomically classified injuries to the PNS

A

Mononeuropathy and Polyneuropathy

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2
Q

What occurs in mononeuropathy

A

Damage to a single nerve or nerve group

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3
Q

What occurs in polyneuropathy

A

Damage occurs to multiple nerves, often symmetrically affecting bilat. of the body

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4
Q

What are etiological classifications for injuries to the PNS

A

Traumatic
Metabolic
Infections / inflammatory
Toxic / chemical

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5
Q

What is an example infection injury to the PNS

A

Infections such as meningitis

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6
Q

What are traumatic injuries to the PNS

A

Injuries caused by external forces and accidents

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7
Q

What are metabolic injuries to the PNS

A

Injuries resulting from systematic conditions such as diabetes, nutritional deficiencies and poisoning

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8
Q

What are infections or inflammatory injuries to the PNS

A

Injuries caused by infections or autoimmune reactions such as meningitis or MS

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9
Q

What are toxic/chemical injuries to the PNS

A

Injuries induced by exposure to toxins or chemicals

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10
Q

What are physiologically classified injuries affecting the PNS

A

Axonopathies
Myelopathies
Vasculopathy

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11
Q

What are axonopathy injuries to the PNS

A

Injuries primarily affecting the axons of the nerves

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12
Q

What are myelopathy injuries of the PNS

A

Injuries affecting the myelin sheath surrounding the nerves, disrupting signal transmissions

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13
Q

What are vasculopathy injuries to the PNS

A

Injuries affecting the blood vessels supplying the nerves, potentially leading to ischaemic conditions

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14
Q

What is the aetiology of Guillian-Barre Syndrome (GBS)

A

Bacterial infection or viral infection
Molecular mimicry can be a probable underlying mechanism

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15
Q

What is the pathophysiology of GBS

A

GBS is an immune-mediated polyradiculoneuropathy with forms including AIDP, ANAN and ASMAN. Each form has unique clinical, pathological and pathophysiological

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16
Q

What is the presentation of GBS

A

Classic GBS is an acute onset ascending sensorimotor neuropathy
Symptoms include (mild to severe)
- Respiratory paralysis
- Autonomic dysfunction

Early diagnosis reduces morbidity and improves prognosis

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17
Q

What are the phases of GBS

A

Acute Phase
Plateau Phase
Recovery Phase

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18
Q

What is involved in the acute phase of GBS

A

Rapid onset of symptoms
Escalates over a period of days or weeks

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19
Q

what occurs in the plateau phase of GBS

A

Stabilisation of symptoms
No further deterioration

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20
Q

What occurs in the recovery phase of GBS

A

Gradual improvement
potential full recovery
May lead to residual deficits

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21
Q

How is GBS diagnosed

A

Based on a combination of medical history, physical exam and tests like CSF examination, electrodiagnostic studies, MRIs, CTs, CT taps

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22
Q

What features are required for diagnosis of GBS

A

Progressive bilateral weakness of arms and legs
Absent or decreased tendon reflexes in affected limbs

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23
Q

What features support diagnosis of GBS

A

progressive phase lasts from days to 4 weeks (usually <2 weeks)
Relative symmetry of symptoms and signs
Relatively mild sensory symptoms and signs (absent in pure motor variant)
Cranial nerve involvement, especially bilateral facial palsy
Autonomic dysfunction
Muscular or radicular back or limb pain
Increased protein level in cerebrospinal fluid (CSF); normal protein levels do not rule out the diagnosis
Electrodiagnostic features of motor or sensorimotor neuropathy (normal electrophysiology in the early stages does not rule out the diagnosis)

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24
Q

What is involved in the acute management of GBS

A

Intravenous immunoglobulin (Ivlg) and plasma exchange are equally effective in treating GBS (only proven effective treatments)

Steroids, plasmapheresis and DVT prophylaxis may also aid

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25
When should GBS patients be admitted to ICU
If have one or more: rapid progression of weakness severe autonomic or swallowing dysfunction evolving respiratory distress EGRIS >4
26
When should treatment be started for GBS
one or more - inability to walk >10m independently - Rapid progression of weakness - severe autonomic or swallowing dysfunction - respiratory insufficiency
27
What is involved in monitoring of GBS
Regularly assessing muscle strength, respiratory function, swallowing function, autonomic function (BP, HR/rhythm, bladder/bowel control)
28
What are possible early complications of GBS
choking arrhythmias infections DVT pain delirium depression urinary retention constipation corneal ulceration dietary deficiency hyponatraemia pressure ulcers compression neuropathy limb contractures
29
What may occur when a GBS patient clinically deteriorates
Suffer from respiratory muscle weakness leading to airway protection loss, ineffective cough, several pulmonary complications Affects respiratory muscles of 40% of patients and may cause neuromuscular respiratory failure in 25%
30
How is respiratory function measured in GBS patients
With bedside pulmonary function Should also monitor for bulbar paulsy and dysautonomia as these can both impair ability to clear secretions, increasing risk of respiratory failure and pulmonary infections
31
what a laboratory markers of failing respiration?
Oxygen saturation less than 92%, pO2 <8kPa, CO2 <6kPa FVC 30% of FVC from baseline within 24 hours inconsistent or falling values of FVC at a single test session A decline in vital capacity by more than 15-20%in the supine position
32
What monitoring is suggested for patients with acute GBS
4 hour forced vital capacity (FVC) 4 hourly pulse, BP, SpO2 Check ABGs (1-2 hourly if FVC <20ml/Kg BW)
33
What are the traumatic causes of spinal cord injuries
Car accidents falls violence and assaults sports and recreational injuries work-related
34
what are non-traumatic causes of spinal cord injuries
vascular disorders infectious diseases degenerative diseases neoplasma developmental disorders autoimmune disorders latrogenic causes
35
other causes of spinal cord injuries
nutritional deficiencies radiation
36
describe the cascade of events during a SCI
Immediate (seconds): - haemorrhage - decreased ATP - increased lactate Early acute (hours): - vasogenic oedema - ion imbalance - Release of neurotoxic opioids - Inflammation - lipid peroxidation - glutamate excitotoxicity - cytotoxic oedema - free radical formation Subacute (days/ weeks) - microglial activation - macrophage activation - cellular apoptosis
37
What is involved in acute managment of SCI
Spinal surgery: - Initial evaluation with neurological exam including spinal reflexes - evaluation of spinal imaging If scans demonstrate compressive force on spinal cord with incomplete cord injury: - urgent decompression with or w/out arthrodesis within 24 hrs If exam beings to show active decline, decompression becomes emergent. If incomplete injury or other systemic injuries prevent safe operative intervention then patient is admitted to ICU for medical management. Obtain MRI of relevant region without contrast unless contraindicated
38
what is key postoperative or peri-injury management for SCI
Early physio early nutritional support with involvement of nutritional consult service removal of foley catheter as soon as tolerated pneumococcus and influenza vaccinations continued chest physiotherapy daily continuation of MAP goal >85 5-7 days
39
What occurs post surgery or conservative management decisions
chest physio goals early mobility as able preventions of deterioration
40
What are types of spinal cord lesions
Tetraplegia Paraplegia Complete / incomplete lesions
41
what are possible clinical syndromes post SCI
Lateral Syndrome Anterior syndrome CES Posterior syndrome Conus medullaris syndrome
42
What is used in immediate medical management
Surgical stabilisation Immobilisation and transportation e.g. aspen collars
43
How can body function and structure be assessed
ASIA assessment
44
What are possible respiratory complications post SCI
Preserving airways Breathing Impaired respiratory capacity Retained secretiosn Autonomic function
45
What may be needed if there are issues preserving airways
may require invasive or non-invasive ventilation
46
How does breathing complication occur due to SCI
Damage to T8 paralyzes intercostal muscles and diaphragm (C3) Injuries at C5 or above can cause failure leading to intubation Lower cervical injuries spare the diaphragm but paralyze the intercostals causing chest to draw in during inhalation - this causes rapid decrease in vital capacity, functional capacity and rapid desaturation
47
How may respiratory capacity be impaired
decreased respiratory muscle strength fatigue paradoxical chest wall movement > effort breathing decreased resp capacity atelectasis Chest wall rigidity
48
Why may there be increased retained secretions
increased secretion production decreased cough effectiveness
49
What may be associated with autonomic dysfunction
increased secretions Bronchospasm Pulmonary oedema
50
what is a possible flow of events that may occurs leading to complication in above T6 paralysis?
-> lack of abdominal innervation -> weak/absent cough -> sputum retention -> infection risk -> aspiration risk
51
what are possible resources for SCI respiratory management
NIV Cough assist Manual assisted cough Secretion management to/ suctioning
52
What may be used to aid in visualisations and turning for the spine
Postural allignment This can be a variety of specialist pillows, splints, elevation, bed types
53
what are possible blood pressure issues whihc may arise
Hypotension Blood pressure instability
54
what is the figure for hypotension
hypotension = systolic BP ≤ 110mmHg for men and ≤100 mmHg for females
55
what is orthostatic hypotension (OH)?
sustained reduction of systolic BP of at least 20 mmHg or diastolic BP of at least 10 mmHg within 3-min of standing or 60 degree head-up tilt OH is frequently found in ppl with autonomic dysfunction
56
What are symptoms of OH
orthostatic intolerance - fatigue - weakness - light headedness - dizziness - blurred vision - headache
57
What are non-pharmacological options for managing hypotension and OH
Exercise functional electrical stimulation compression stockings abdominal binders
58
what is BP instability
unpredictable BP changes that can occur frequently but often go unnotives by both pt and clinical
59
What is autonomic dysreflexia (AD)
found in adults with SCI at or above T6 that causes elevated systolic BP greater than 20 mmHG above usual base line Many individuals report few or no symptoms
60
what are possible symptoms of AD
Many dont experience symptoms but may be headache change in HR profuse sweating on face, neck and shoulder piloerection blurred vision nasal congestion feelings of anxiety
61
What is spasticity
Exaggeration of stretch reflex caused by hyperexcitability of spinal reflexes in upper motor neuron syndrome
62
How does spasticity occur in SCI
Post SCI period of flaccid muscle paralysis and loss of tendon reflexes = spinal shock lasts 1-3 days to few weeks this is followed by exaggerated tendon reflexes, increased muscle tone and muscle spasms or spasticity
63
How can spasticity be managed
positioning ROM + stretching and splinting/orthoses Weight bearing muscle strengtheningh
64
how does positioning aid spasticity
maintenance of muscle length
65
How does ROM and stretching and splinting/orthoses
prevention of contractures; long-term stretch; causes temporary reduction in intensity of muscle contraction in reaction to muscle stretch
66
how does weight bearing improve spasticity
Prolonged stretch of ankle plantar flexor muscles
67
How does muscle strengthening aid spasticity
Emphasis of balance of agonist and antagonist groups of muscles and voluntary control
68
what is the timing of rehabilitation for acute SCI
rehab can be offered to patients with acute SCI once medically stable and can tolerate required rehab intensity any recommendation would be based on indirect evidence or clinical expert opinion
69
what are the goals of acute rehab post SCI
increase strength treat and prevent contractures and muscle changes improve the performance/function of motor tasks Improve sensorial integration and sensation
70
What is the role of OT in SCI
Sitting ax w/chair ax orthosis functional task and ADL practice engagement / motivation and social pptcian adapting environment, support joint decision making
71
what is the role of ns and medicine in SCI
weaning from non + invasive ventilation tracheostomy management sittining management pressure sore management transfers and mobility spasticity and tone management respiratory management
72
what is the role of SaLT in SCI care
sitting optimisation for sport and E+D communication management of trachi : weaning from trache and ventilation, FEES and swallowing

Acute Care and Rehab (8 decks)

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