neuro conditions Flashcards
What are anatomically classified injuries to the PNS
Mononeuropathy and Polyneuropathy
What occurs in mononeuropathy
Damage to a single nerve or nerve group
What occurs in polyneuropathy
Damage occurs to multiple nerves, often symmetrically affecting bilat. of the body
What are etiological classifications for injuries to the PNS
Traumatic
Metabolic
Infections / inflammatory
Toxic / chemical
What is an example infection injury to the PNS
Infections such as meningitis
What are traumatic injuries to the PNS
Injuries caused by external forces and accidents
What are metabolic injuries to the PNS
Injuries resulting from systematic conditions such as diabetes, nutritional deficiencies and poisoning
What are infections or inflammatory injuries to the PNS
Injuries caused by infections or autoimmune reactions such as meningitis or MS
What are toxic/chemical injuries to the PNS
Injuries induced by exposure to toxins or chemicals
What are physiologically classified injuries affecting the PNS
Axonopathies
Myelopathies
Vasculopathy
What are axonopathy injuries to the PNS
Injuries primarily affecting the axons of the nerves
What are myelopathy injuries of the PNS
Injuries affecting the myelin sheath surrounding the nerves, disrupting signal transmissions
What are vasculopathy injuries to the PNS
Injuries affecting the blood vessels supplying the nerves, potentially leading to ischaemic conditions
What is the aetiology of Guillian-Barre Syndrome (GBS)
Bacterial infection or viral infection
Molecular mimicry can be a probable underlying mechanism
What is the pathophysiology of GBS
GBS is an immune-mediated polyradiculoneuropathy with forms including AIDP, ANAN and ASMAN. Each form has unique clinical, pathological and pathophysiological
What is the presentation of GBS
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
What are the phases of GBS
Acute Phase
Plateau Phase
Recovery Phase
What is involved in the acute phase of GBS
Rapid onset of symptoms
Escalates over a period of days or weeks
what occurs in the plateau phase of GBS
Stabilisation of symptoms
No further deterioration
What occurs in the recovery phase of GBS
Gradual improvement
potential full recovery
May lead to residual deficits
How is GBS diagnosed
Based on a combination of medical history, physical exam and tests like CSF examination, electrodiagnostic studies, MRIs, CTs, CT taps
What features are required for diagnosis of GBS
Progressive bilateral weakness of arms and legs
Absent or decreased tendon reflexes in affected limbs
What features support diagnosis of GBS
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)
What is involved in the acute management of GBS
Intravenous immunoglobulin (Ivlg) and plasma exchange are equally effective in treating GBS (only proven effective treatments)
Steroids, plasmapheresis and DVT prophylaxis may also aid
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
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
What is involved in monitoring of GBS
Regularly assessing muscle strength, respiratory function, swallowing function, autonomic function (BP, HR/rhythm, bladder/bowel control)
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
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%
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
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
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)
What are the traumatic causes of spinal cord injuries
Car accidents
falls
violence and assaults
sports and recreational injuries
work-related
what are non-traumatic causes of spinal cord injuries
vascular disorders
infectious diseases
degenerative diseases
neoplasma
developmental disorders
autoimmune disorders
latrogenic causes
other causes of spinal cord injuries
nutritional deficiencies
radiation
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
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
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
What occurs post surgery or conservative management decisions
chest physio
goals
early mobility as able
preventions of deterioration
What are types of spinal cord lesions
Tetraplegia
Paraplegia
Complete / incomplete lesions
what are possible clinical syndromes post SCI
Lateral Syndrome
Anterior syndrome
CES
Posterior syndrome
Conus medullaris syndrome
What is used in immediate medical management
Surgical stabilisation
Immobilisation and transportation
e.g. aspen collars
How can body function and structure be assessed
ASIA assessment
What are possible respiratory complications post SCI
Preserving airways
Breathing
Impaired respiratory capacity
Retained secretiosn
Autonomic function
What may be needed if there are issues preserving airways
may require invasive or non-invasive ventilation
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
How may respiratory capacity be impaired
decreased respiratory muscle strength
fatigue
paradoxical chest wall movement > effort breathing
decreased resp capacity
atelectasis
Chest wall rigidity
Why may there be increased retained secretions
increased secretion production
decreased cough effectiveness
What may be associated with autonomic dysfunction
increased secretions
Bronchospasm
Pulmonary oedema
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
what are possible resources for SCI respiratory management
NIV
Cough assist
Manual assisted cough
Secretion management to/ suctioning
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
what are possible blood pressure issues whihc may arise
Hypotension
Blood pressure instability
what is the figure for hypotension
hypotension = systolic BP ≤ 110mmHg for men and ≤100 mmHg for females
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
What are symptoms of OH
orthostatic intolerance
- fatigue
- weakness
- light headedness
- dizziness
- blurred vision
- headache
What are non-pharmacological options for managing hypotension and OH
Exercise
functional electrical stimulation
compression stockings
abdominal binders
what is BP instability
unpredictable BP changes that can occur frequently but often go unnotives by both pt and clinical
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
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
What is spasticity
Exaggeration of stretch reflex caused by hyperexcitability of spinal reflexes in upper motor neuron syndrome
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
How can spasticity be managed
positioning
ROM + stretching and splinting/orthoses
Weight bearing
muscle strengtheningh
how does positioning aid spasticity
maintenance of muscle length
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
how does weight bearing improve spasticity
Prolonged stretch of ankle plantar flexor muscles
How does muscle strengthening aid spasticity
Emphasis of balance of agonist and antagonist groups of muscles and voluntary control
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
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
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
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
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
